Myocardial Infarction; Causes, Symptoms, Diagnosis, Treatment

Myocardial infarction








User Review


4.92
(12 votes)


Myocardial infarction also called a heart attack happens when a blood vessel in the heart suddenly becomes blocked. Blood vessels carry blood and oxygen. When a blood vessel in the heart gets blocked, blood cannot get to the part of the heart. This part of the heart does not get enough oxygen. This is called ischemia. When the heart muscle becomes ischemic (does not get enough blood and oxygen), the ischemia often causes chest pain. This is called angina pectoris. If the ischemia lasts long enough, the heart muscle that is not getting enough oxygen dies. This is called an infarction. “Myocardial infarction” means “infarction (muscle death) in the heart muscle.

Myocardial infarction (MI) is a term used for an event of a heart attack which is due to the formation of plaques in the interior walls of the arteries resulting in reduced blood flow to the heart and injuring heart muscles because of lack of oxygen supply. The symptoms of MI include chest pain, which travels from left arm to neck, shortness of breath, sweating, nausea, vomiting, abnormal heart beating, anxiety, fatigue, weakness, stress, depression, and other factors. The immediate treatment of MI include taking aspirin, which prevents blood from clotting, and nitro-glycerin to treat chest pain and oxygen. The heart attack can be prevented by taking an earlier action to lower those risks by controlling diet, fat, cholesterol, salt, smoking, nicotine, alcohol, drugs, monitoring of blood pressure every week, doing exercise every day, and losing body weight. The treatment of MI includes, aspirin tablets, and to dissolve arterial blockage injection of thrombolytic or clot-dissolving drugs such as tissue plasminogen activator, streptokinase or urokinase in blood within 3 h of the onset of a heart attack. The painkillers such as morphine or meperidine can be administered to relieve pain. Nitroglycerin and antihypertensive drugs such as beta-blockers, ACE inhibitors or calcium channel blockers may also be used to lower blood pressure and to improve the oxygen demand of heart. The ECG, coronary angiography and X-ray of heart and blood vessels can be performed to observe the narrowing of coronary arteries. [Rx]

A heart attack is a medical emergency. The first few minutes are very important for keeping the person alive. Some of the damage from the heart attack can be repaired if the person gets treatment during the first hour of the attack

Types of Myocardial Infarction

Third universal classification of myocardial infarction

Type 1: Spontaneous MI
  • Spontaneous MI due to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have underlying severe CAD, non-obstructive coronary disease or no CAD
Type 2: MI secondary to an ischemic imbalance
  • Myocardial injury with necrosis occurs due to conditions other than CAD that contribute to an imbalance between myocardial oxygen supply and/or demand such as coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachycardia-bradycardia arrhythmias, anemia, respiratory failure, hypotension, and hypertension
Type 3: MI resulting in death when biomarker values are unavailable
  • Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes or new LBBB, but death occurs before blood samples can be obtained before cardiac troponins biomarkers rise, or when cardiac biomarkers were not collected
Type 4A: MI related to percutaneous coronary intervention
  • I associated with PCI is defined by elevation of cTn values greater than five times the 99th percentile upper normal reference limit (URL) in patients with normal baseline values (< 99th percentile URL) or a rise of cTn values by > 20% if the baseline troponins are elevated and are stable or falling. In addition one of the following criterion are required: (1) symptoms suggestive of myocardial ischemia; (2) new ischemic ECG changes or new LBBB; (3) angiographic loss of patency of a major coronary artery or a side branch or persistent slow- or no coronary flow or coronary embolization; or (4) demonstration with imaging of a new loss of viable myocardium or new regional wall motion abnormality
Type 4B: MI related to stent thrombosis
  • I associated with stent thrombosis detected by coronary angiography or autopsy in the presence of myocardial ischemia with a rise and/or fall of troponin biomarkers. One troponin measurement should be above the 99 percentile UR
Type 4C: MI related to restenosis
  • I associated with restenosis defined as ≥ 50% stenosis or a complex lesion demonstrated at coronary angiography after (1) initial successful stent deployment; or (2) dilatation of a coronary artery stenosis with balloon angioplasty. These coronary angiographic changes should be associated with an increase and/or decrease of cTn values > 99th percentile URL and no other significant obstructive CAD
Type 5: MI related to coronary artery bypass grafting
  • MI associated with CABG is defined by elevation of cardiac troponins greater than ten times the 99thpercentile URL in patients with normal baseline cTn values (< 99th percentile URL). In addition, one of the following should be present: (1) new pathological Q waves or new LBBB; or (2) angiographic documented new graft or new native coronary artery occlusion; or (3) new loss of viable myocardium or new regional wall motion abnormality as shown by an imaging modality

Myocardial infarction is classified into two types

  • ST-segment elevation myocardial infarction (STEMI) – It occurs by complete occlusion of a major coronary artery that produces entire thickness damage of heart muscle. STEMI is also called transmural infarction due to its full thickness involvement. This entire thickness damage of heart muscle produces an ECG (electrocardiography) change of ST-segment elevation. It can be subclassified into anterior, anteroseptal, posterior, inferior, lateral, high lateral or anterolateral myocardial infarction (according to left ventricular wall damage), and RV type (according to right ventricular wall damage).
  • Non-ST-segment elevation myocardial infarction (NSTEMI) – NSTEMI is usually due to complete occlusion of a minor coronary artery or partial occlusion of a major coronary artery that produces partial thickness damage of heart muscle. Here, the damage of heart muscle is confined to the inner ⅓ rd – ⅔ rd of the left ventricular wall. For this reason, it is also called subendocardial infarction. ST-segment elevation in ECG is not developed in this myocardial infarction because of partial thickness damage of heart muscle. Here, this muscle damage is demonstrated by an elevation of cardiac markers (CK-MB or Troponin) in the blood.

Types

Myocardial infarctions are generally clinically classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). These are based on changes to an ECG.[Rx] STEMIs make up about 25 – 40% of myocardial infarctions.[Rx] A more explicit classification system, based on international consensus in 2012, also exists. This classifies myocardial infarctions into five types:[Rx]

  • Spontaneous MI related to plaque erosion and/or rupture, fissuring, or dissection
  • MI related to ischemia, such as from increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, high blood pressure or low blood pressure
  • Sudden unexpected cardiac death, including cardiac arrest, where symptoms may suggest MI, an ECG may be taken with suggestive changes, or a blood clot is found in a coronary artery by angiography and/or at autopsy, but where blood samples could not be obtained, or at a time before the appearance of cardiac biomarkers in the blood
  • Associated with coronary angioplasty or stents
    • Associated with percutaneous coronary intervention (PCI)
    • Associated with stent thrombosis as documented by angiography or at autopsy
  • Associated with CABG
  • Associated with spontaneous coronary artery dissection in young, fit women

Causes of Myocardial Infarction

The factors that lead to anterior MI are similar to those causing damage in other parts of the heart which are supplied by other branches of the coronary arteries. Risk factors which may predispose one to develop a heart attack include

  • Age greater than 45 years (although younger people may also experience it)
  • The family history of heart attack
  • Male gender
  • Smoking
  • High cholesterol levels in the blood
  • High blood pressure that is poorly controlled
  • Type A personality
  • Lack of exercise

Causes of anterior MI as well as in any part of the heart include

  • Atherosclerosis leading to plaque formation in the coronary arteries – the most common cause
  • Coronary artery vasospasm (constriction)
  • Embolism or blood clots
  • Carbon monoxide poisoning
  • Left ventricular hypertrophy (enlargement)
  • Drugs containing cocaine, amphetamines, and ephedrine
  • Arteritis
  • Aortic dissection
  • A coronary aneurysm

Symptoms of Myocardial Infarction

A heart attack involving the left ventricle can compromise the pumping action of the heart and the blood supply to the rest of the body. This can lead to symptoms like:

  • Chest pains – constricting, stabbing, squeezing type of pain under the breastbone or the left side of the chest; pains may radiate to the neck, back, shoulder and left arm
  • Shortness of breath or difficulty in breathing
  • Lightheadedness may be accompanied by fainting
  • Anxiety and a sense of impending doom
  • Extreme paleness, with cold and clammy skin
  • General weakness or fatigue
  • Squeezing pain, heaviness, tightness, pressure in the center of the chest
  • Pain that spreads to your back, left arm, jaw, neck
  • Dizziness, weakness
  • Nausea, vomiting
  • Irregular heartbeat
  • Sweating
  • Feeling of doom

Women may experience different symptoms than men. In women, along with chest pain, symptoms can include:

  • Heartburn or pain in the abdomen
  • Unusual fatigue
  • Clammy skin

Women’s symptoms sometimes differ

Although most women and men report symptoms of chest pain with a heart attack, women are slightly more likely than men to report unusual symptoms. Those who have more vague or less typical “heart” symptoms have reported the following:

  • Upper back or shoulder pain
  • Jaw pain or pain spreading to the jaw
  • Pressure or pain in the center of the chest
  • Light headaches
  • Pain that spreads to the arm
  • Unusual fatigue for several days

Risk factors for Myocardial Infarction

The following risk factors have been associated with a higher incidence of myocardial infarction. Some of these risk factors are controllable (such as smoking and physical activity) while others are uncontrollable (such as age, genetics, family history).

  • Age –  Four out of five patients with coronary artery disease are 65 years of age or older. After menopause, females are more likely to die within the first year of having a myocardial infarction than males.
  • Gender –  Males are at higher risk of myocardial infarction than women, and males are also more likely to suffer myocardial infarction earlier in life. However, heart disease kills more females each year than any other disease, including breast cancer. An alarming survey reported by the American Heart Association found that only 8% of women perceive heart disease as the greatest threat to their health despite the fact that heart disease is the leading cause of death among both women and men. Over 500,000 American women die from cardiovascular disease each year twice the number of deaths from all cancers combined. Also, women are more likely to die within the first year of a heart attack than men.
  • Family history/race –  A family history of heart disease increases the risk of coronary artery disease and myocardial infarction. In the United States, African Americans tend to have more severe high blood pressure than Caucasians, increasing coronary artery disease/myocardial infarction risk. The incidence of heart disease is also higher among certain population groups such as Mexican Americans, American Indians, native Hawaiians, and some Asian Americans.
  • Smoking –  Cigarette smokers are twice as likely to experience myocardial infarction compared to non-smokers. Smokers also have a two to four time higher risk of sudden cardiac death (within an hour of a heart attack).
  • High blood pressure (hypertension) –  Alone or in association with obesity, smoking, high blood cholesterol levels or diabetes, high blood pressure increases the risk of myocardial infarction and stroke.
  • High blood cholesterol – High total and low-density lipoprotein (LDL cholesterol) levels and low HDL cholesterol levels increase the risk of myocardial infarction Cholesterol levels can be lowered with dietary/lifestyle modifications such as exercise or medications.
  • Obesity – Obesity increases coronary artery disease, myocardial infarction, and stroke risk. Obesity increases strain on the heart, raises blood pressure and cholesterol, and increases diabetes risk. Weight reduction can be achieved with modifications to diet and increased physical activity.
  • Diabetes – Approximately two-thirds of patients with diabetes die from heart or blood vessel disease. Adults with diabetes are three to seven times more likely to develop heart disease. A recent recommendation from the U.S. government advocates aggressive treatment of high cholesterol in people with diabetes.
  • Lack of physical activity – Regular exercise reduces the risk of coronary artery disease and myocardial infarction by controlling blood cholesterol levels, decreasing the risk of obesity or diabetes, and lowering blood pressure levels in some patients.
  • Stress –  Research indicates a possible relationship between stress and coronary artery disease, which may lead to myocardial infarction Hypertension (high blood pressure) and high cholesterol are associated with stress, as are increased tendencies to smoke, gain weight and/or decrease physical activity.

Diagnosis of Myocardial Infarction

Treating a heart attack quickly can save your life, while delay can be fatal. In the emergency room, a doctor will ask you about your symptoms and perform a physical examination. The doctor will immediately run tests to determine your heart function. They may include

  • Echocardiogram (heart ultrasound) – This diagnostic technique is an excellent first step in investigating congenital heart disease or in evaluating abnormalities of the heart wall. Echocardiography is a non-invasive exam in which images are acquired and viewed in real time without the use of radiation. Echocardiography is often useful in studying the beating heart and provides some information on the functional abnormalities of the heart wall, valves, and blood vessels. Doppler ultrasound can be used to measure blood flow across a heart valve. Abnormal operation of the valves can be detected by studying the opening and closing function versus normal valve function. Echocardiography may also be used to study congenital heart defects such as a septal defect (a hole in the wall that separates the two chambers of the heart).
  • Blood tests – Your doctor may look for certain enzymes that are released into your blood when you have a heart attack.

Other tests include

  • CBC, ESR,Hb
  • Serum cholesterol, C-reactive protein, Serum creatine,
  • Chest x-ray
  • Echocardiogram – (uses sound waves to take a picture of your heart)
  • Coronary catheterization or angiogram –  (uses a liquid dye inserted through a catheter to see whether your arteries are blocked)
  • Stress test –  (involves walking on a treadmill while hooked up to an ECG machine to see how your heart responds to exercise)
  • Coronary angiogram – an x-ray imaging technique to show if the coronary arteries are narrowed or blocked
  • Exercise stress test –  involves conducting an ECG during exercise since problems with the heart are more likely to be revealed when the heart is working harder
  • Cardiac computerized tomography (CT) – or magnetic resonance imaging (MRI), involves the use of high-tech machines to reveal problems with the heart and coronary arteries by taking a series detailed images of the heart.
  • Nuclear medicine –  Nuclear medicine (also called radionuclide scanning) allows visualization of the anatomy and function of an organ. The patient will be given a radionuclide which will assist in the acquisition of clear images of the heart with a gamma camera. Nuclear medicine imaging may be used to detect coronary artery disease, myocardial infarction, valve disease, heart transplant rejection, check the effectiveness of bypass surgery, or to select patients for angioplasty or coronary bypass graft.

Treatment of Myocardial Infarction

  • Arrange an emergency ambulance if an AMI is suspected – Take an ECG as soon as possible but do not delay transfer to hospital, as an ECG is only of value in pre-hospital management if pre-hospital thrombolysis is being considered.
  • Advise any patient known – to have coronary heart disease to call for an emergency ambulance if the chest pain is unresponsive to glyceryl trinitrate (GTN) and has been present for longer than 15 minutes or on the basis of general clinical state – eg, severe dyspnoea or pain.
  • Cardiopulmonary resuscitation – and defibrillation in the event of a cardiac arrest.
  • Oxygen – do not routinely administer oxygen but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to
  • People with oxygen saturation – less than 94% who are not at risk of hypercapnic respiratory failure, aiming for saturation of 94-98%.
  • People with the chronic obstructive pulmonary disease – who are at risk of hypercapnic respiratory failure, to achieve a target saturation of 88-92% until blood gas analysis is available.
  • Pain relief with GTN sublingual/spray and/or –  an intravenous opioid 2.5-5 mg diamorphine or 5-10 mg morphine intravenously with an anti-emetic.Avoid intramuscular injections, as absorption is unreliable and the injection site may bleed if the patient later receives thrombolytic therapy.
  • Aspirin 300 mg orally – (dispersible or chewed).
  • Insert a Venflon for intravenous access and take blood tests for FBC, – renal function and electrolytes, glucose, lipids, clotting screen, C-reactive protein (CRP) and cardiac enzymes (troponin I or T).
  • Pre-hospital thrombolysis is indicated – if the time from the initial call to arrival at the hospital is likely to be over 30 minutes. When primary percutaneous coronary intervention cannot be provided within 120 minutes of ECG diagnosis, patients with an ST-segment-elevation acute coronary syndrome should receive immediate (pre-hospital or admission) thrombolytic therapy.
  • National Institute for Health and Care Excellence (NICE) – recommends using intravenous bolus (reteplase or tenecteplase) rather than an infusion for pre-hospital thrombolysis.
  • The goals of therapy in acute MI – are the expedient restoration of normal coronary blood flow and the maximum salvage of functional myocardium. These goals can be met by a number of medical interventions and adjunctive therapies. The primary obstacles to achieving these goals are the patient’s failure to recognize MI symptoms quickly and the delay in seeking medical attention. When patients present to a hospital, there are a variety of interventions to achieve treatment goals. “Time is muscle” guides the management decisions in acute STEMI, and an early invasive approach is the standard of care for acute NSTEMI.

Medical Options

  • Aspirin Helps stop blood from clotting. You may be given aspirin in the ambulance or as soon as you get to the hospital. Aspirin should be continued indefinitely at a dose of 81 mg per day, or as directed by your physician.
  • Warfarin (INR 2-3) – or dabigatran can be considered for patients unable to take aspirin or clopidogrel.
  • Nitroglycerin – Helps dilate (widen)or used to widen your blood vessels. You may be given nitroglycerin in the ambulance or as soon as you get to the hospital.
  • Pain reliever Helps relieve pain and is often given intravenously (IV).
  • Thrombolytics – Work to break up clots. They are most effective when taken within 2 hours of the heart attack, and are not given after 12 hours have elapsed. These drugs may be given with other anticoagulants (blood thinners).
  • Anticoagulants (blood thinners) – Make your blood less likely to form clots. Heparin is often given by injection while you are in the hospital..
  • Antiplatelet – drugs, such as clopidogrel, can be used to prevent new clots from forming and existing clots from growing.
  • Beta-blockers – lower your blood pressure and relax your heart muscle. This can help limit the severity of damage to your heart.
  • ACE inhibitors – can also be used to lower blood pressure and decrease stress on the heart.
  • Bronko dilator – group of medicine(montelukast) can be used to accelerate the normal breathing.
  • Anti-depressants – the drug can be used to sleep normally.
  • Antibiotic & prednisolone/methylprednisolone –  in some cases can be used to erase the inflammation in the supervision of a cardiologist.
  • Lipid-lowering agent – (atorvastatin, pitavastatin)can be used in case of controlling blood pressure & removed excess fat from the body.

Other Treatment

  • Heparin infusion is used as an adjunctive agent in patients receiving alteplase but not with streptokinase. Heparin is also indicated in patients undergoing primary angioplasty.
  • Prophylaxis against thromboembolism: if not already receiving heparin by infusion, then patients should be given regular subcutaneous heparin until fully mobile.
  • Insulin-glucose infusion followed by intensive glucose control with subcutaneous insulin for all people with type 1 and type 2 diabetes.
  • The routine use of nitrates, calcium antagonists, magnesium, and the high-dose glucose-insulin-potassium infusion is not currently recommended during the acute phase of treatment of AMI.

Antiplatelet Agents

  • The use of aspirin has been shown to reduce mortality from MI. Aspirin in a dose of 325 mg should be administered immediately on recognition of MI signs and symptoms. The nidus of an occlusive coronary thrombus is the adhesion of a small collection of activated platelets at the site of intimal disruption in an unstable atherosclerotic plaque.
  • Aspirin irreversibly interferes with the function of cyclooxygenase and inhibits the formation of thromboxane A2. Within minutes, aspirin prevents additional platelet activation and interferes with platelet adhesion and cohesion. This effect benefits all patients with acute coronary syndromes, including those with amyocardial infarction. Aspirin alone has one of the greatest impacts on the reduction of MI mortality.
  • Its beneficial effect is observed early in therapy and persists for years with continued use. The long-term benefit is sustained, even at doses as low as 75 mg/day.

Statins  – Help lower cholesterol. People who are pregnant or have liver disease should not take statins. They include:

  • Lovastatin (Mevacor)
  • Simvastatin (Zocor)
  • Pravastatin (Pravachol)
  • Atorvastatin (Lipitor)
  • Fluvastatin (Lescol)
  • Rosuvastatin (Crestor)

Niacin (nicotinic acid)  – In prescription form, is sometimes used to lower cholesterol. Dietary supplements of niacin should not be used instead of prescription niacin, as it can cause side effects. Take niacin for high cholesterol only with your doctor’s supervision.

Table 1: Antiplatelet Medications

Treatment Modality Aspirin Clopidogrel
Medical management 75-162 mg/day indefinitely Optional: 75 mg/day × 1 month
Bare Metal stent 162-325 mg/day × 1 month, then 75-162 mg/day indefinitely 300 mg loading dose,* then
75 mg/day × 1 month
Sirolimus-eluting stent
(Cypher)
162-325 mg/day × 3 months, then 75-162 mg/day indefinitely 300 mg loading dose,* then
75 mg/day × 1 year
Paclitaxel-eluting stent
(Taxus)
162-325 mg/day × 6 months, then 75-162 mg/day indefinitely 300 mg loading dose,* then
75 mg/day × 1 year

 * Note: No loading dose in patients older than 75 years.

Supplemental Oxygen

  • Oxygen should be administered to patients with symptoms or signs of pulmonary edema or with pulse oximetry less than 90% saturation. The rationale for using oxygen is the assurance that erythrocytes will be saturated to maximum carrying capacity. Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and by other tissues may be diminished. In some cases, elevated pulmonary capillary pressure and pulmonary edema can decrease oxygen uptake as a result of impaired pulmonary alveolar-capillary diffusion. Supplemental oxygen increases the driving gradient for oxygen uptake.

Nitrates

  • Intravenous nitrates should be administered to patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI. The primary benefit of nitrates is derived from its vasodilator effect. Nitrates are metabolized to nitric oxide in the vascular endothelium. Nitric oxide relaxes vascular smooth muscle and dilates the blood vessel lumen.
  • Vasodilatation reduces cardiac preload and afterload and decreases the myocardial oxygen requirements needed for circulation at a fixed flow rate. Vasodilatation of the coronary arteries improves blood flow through the partially obstructed vessels as well as through collateral vessels. Nitrates can reverse the vasoconstriction associated with thrombosis and coronary occlusion.
  • When administered sublingually or intravenously, nitroglycerin has a rapid onset of action. Clinical trial data have supported the initial use of nitroglycerin for up to 48 hours in MI. There is little evidence that nitroglycerin provides substantive benefit as long-term post-MI therapy, except when severe pump dysfunction or residual ischemia is present. Low BP, headache, and tachyphylaxis limit the use of nitroglycerin. Nitrate tolerance can be overcome by increasing the dose or by providing a daily nitrate-free interval of 8 to 12 hours. Nitrates must be avoided in patients who have taken a phosphodiesterase inhibitor within the previous 24 hours.

Pain Control

  • Pain from MI is often intense and requires prompt and adequate analgesia. The agent of choice is morphine sulfate, given initially IV at 5 to 15 minute intervals at typical doses of 2 to 4 mg. Reduction in myocardial ischemia also serves to reduce pain, so oxygen therapy, nitrates, and beta blockers remain the mainstay of therapy. Because morphine can mask ongoing ischemic symptoms, it should be reserved for patients being sent for coronary angiography. This was downgraded to a IIa recommendation in the latest STEMI guidelines.

Beta Blockers

  • Beta-blocker therapy is recommended within 12 hours of MI symptoms and is continued indefinitely. Treatment with a beta blocker decreases the incidence of ventricular arrhythmias, recurrent ischemia, reinfarction, and, if given early enough, infarct size and short-term mortality. Beta blockade decreases the rate and force of myocardial contraction and decreases overall myocardial oxygen demand. In the setting of reduced oxygen supply in MI, the reduction in oxygen demand provided by beta-blockade can minimize myocardial injury and death (Table 2).

Table 2: Beta-Blocker Therapy

Agent Dosing Original Trial
Metoprolol 15 mg IV × 1 then 200 mg/day PO in divided doses MIAMI
Atenolol 5-10 mg IV × 1, then 100 mg/day PO ISIS-1
Carvedilol 6.25 mg bid titrated to 25 mg BID CAPRICORN

ISIS-1, International Studies of Infarct Survival-1; MIAMI, Metoprolol in Acute Myocardial Infarction.

Beta-blockers is a slows heart rate, thus lowering blood pressure. These drugs include:

  • Acebutolol (Sectral)
  • Atenolol (Tenormin)
  • Bisoprolol (Zebeta)
  • Carteolol (Cartrol)
  • Metoprolol (Toprol XL)
  • Nadolol (Corgard)
  • Propranolol (Inderal)

The use of a beta blocker has a number of recognized adverse effects. The most serious are heart failure, bradycardia, and bronchospasm. During the acute phase of an MI, beta blocker therapy may be initiated intravenously; later, patients can switch to oral therapy for long-term treatment. The COMMIT-CCS 2 trial raised safety concerns about the use of early intravenous beta blockers in high-risk patients. In some patients who are considered high risk due to age or hemodynamic instability, it may be reasonable to hold off on early intravenous therapy.

According to the 2007 guideline updates, anticoagulation should be added to standard medical therapy for most patients after myocardial infarction.

Unfractionated Heparin

  • Unfractionated heparin is beneficial until the inciting thrombotic cause (ruptured plaque) has completely resolved or healed. Unfractionated heparin has been shown to be effective when administered intravenously or subcutaneously according to specific guidelines.
  • The minimum duration of heparin therapy after MI is generally 48 hours, but it may be longer, depending on the individual clinical scenario. Heparin has the added benefit of preventing thrombus through a different mechanism than aspirin (Box 1).
Box 1: Unfractionated Heparin Dosing
Loading Dose
  • 60 U/kg IV bolus
  • Max 5000 U if >65 kg or 4000 U if <65 kg
Maintenance Dose
  • 12 U/kg/hr IV
  • Max 1000 U/hr if >65 kg or 800 U/hr if <65 kg
Titration Goal
  • PTT 50-70 sec

PTT, prothrombin time.

Low-Molecular-Weight Heparin

  • Low-molecular-weight heparin (LMWH) can be administered to MI patients who are not treated with fibrinolytic therapy and who have no contraindications to heparin. The LMWH class of drugs includes several agents that have distinctly different anticoagulant effects. LMWHs are proved to be effective for treating acute coronary syndromes characterized by unstable angina and NSTEMI.Their fixed doses are easy to administer, and laboratory testing to measure their therapeutic effect is usually not necessary (Table 3).

Table 3: Low-Molecular-Weight Heparin

Generic name t1/2
(after SC dosing)
Dosing in ACS FDA Approved Indications
Dalteparin 3-5 hr 120 U/kg SC bid Prevention of ischemic complications in UA and NSTEMI
Enoxaparin 4.5 hr 100 U/kg (1 mg/kg) SC q12h Prophylaxis of ischemic complications of UA and NSTEMI when administered with aspirin

UA, unstable angina; NSTEMI, non−ST segment elevation myocardial infarction.

Warfarin

  • Warfarin is not routinely used after MI, but it does have a role in selected clinical settings. The latest guidelines recommend the use of warfarin for at least 3 months in patients with left ventricular aneurysm or thrombus, a left ventricular ejection fraction less than 30%, or chronic atrial fibrillation.

Fibrinolytics

  • Restoration of coronary blood flow in MI patients can be accomplished pharmacologically with the use of a fibrinolytic agent. Fibrinolytic therapy is indicated for patients who present with a STEMI within 12 hours of symptom onset without a contraindication.
  • Absolute contraindications to fibrinolytic therapy include the history of intracranial hemorrhage, ischemic stroke or closed head injury within the past 3 months, the presence of an intracranial malignancy, signs of an aortic dissection, or active bleeding. Fibrinolytic therapy is primarily used at facilities without access to an experienced interventionalist within 90 minutes of presentation.
  • As a class, the plasminogen activators have been shown to restore normal coronary blood flow in 50% to 60% of STEMI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years.
  • The most critical variable in achieving successful fibrinolysis is the time from symptom onset to drug administration. A fibrinolytic is most effective within the first hour of symptom onset and when the door-to-needle time is 30 minutes or less.

Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers

  • Angiotensin-converting enzyme (ACE) inhibitors should be used in all patients with a STEMI without contraindications. ACE inhibitors are also recommended in patients with NSTEMI who have diabetes, heart failure, hypertension, or an ejection fraction less than 40%.
  • In such patients, an ACE inhibitor should be administered within 24 hours of admission and continued indefinitely. Further evidence has shown that the benefit of ACE inhibitor therapy can likely be extended to all patients with an MI and should be started before discharge. Contraindications to ACE inhibitor use include hypotension and declining renal function.

ACE inhibitors  – is widen blood vessels and make it easier for your heart to pump blood. Side effects can include a chronic cough. ACE inhibitors include:

  • Benazepril (Lotensin)
  • Captopril (Capoten)
  • Fosinopril (Monopril)
  • Lisinopril (Zestril)
  • Enlapril (Vasotec)

The most commonly used ACE inhibitors are summarized in table 4.

Table 4: ACE Inhibitors

Agent Dosing (PO) Original Trial
Captopril 6.25 mg tid titrated to 50 mg tid SAVE: 3-16 days post-MI in asymptomatic patients with EF <40%
Ramipril 1.25 mg bid titrated to 5 mg bid AIRE: 3-10 days post-MI with symptoms of heart failure
Captopril 6.25 mg bid titrated to 50 mg bid ISIS-4: started within 24 hr of MI
Lisinopril 5 mg/day titrated to 10 mg/day GISSI-3: started within 24 hr of MI

AIRE, Acute Infarction Ramipril Efficacy; EF, ejection fraction; GISSI-3, Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico; ISIS-4, International Studies of Infarct Survival-1; MI, myocardial infarction; SAVE, Survival and Ventricular Enlargement.

Bile acid sequestrants. Lowers cholesterol; people who have high levels of triglycerides (fats in the blood) should not take bile acid sequestrants. These drugs include:

  • Cholestyramine (Questran)
  • Colestipol (Colestid)
  • Colesevelam (Welchol)

Fabric acid derivatives. Lower triglycerides and moderately lower LDL cholesterol. They include Gemfibrozil (Lopid).

Anticoagulants (blood thinners). Help keep clots from forming. Your doctor may prescribe aspirin, warfarin (Coumadin), or Clopidogrel (Plavix).

  • ACE inhibitors decrease myocardial afterload through vasodilatation. One effective strategy for instituting an ACE inhibitor is to start with a low-dose, short-acting agent and titrate the dose upward toward a stable target maintenance dose at 24 to 48 hours after symptom onset. Once a stable maintenance dose has been achieved, the short-acting agent can be continued or converted to an equivalent-dose long-acting agent to simplify dosing and encourage patient compliance. For patients intolerant of ACE inhibitors, angiotensin receptor blocker (ARB) therapy may be considered.

Glycoprotein IIb/IIIa Antagonists

  • Glycoprotein IIb/IIIa receptors on platelets bind to fibrinogen in the final common pathway of platelet aggregation. Antagonists to glycoprotein IIb/IIIa receptors are potent inhibitors of platelet aggregation.
  • The use of glycoprotein IIb/IIIa inhibitors during the percutaneous coronary intervention (PCI) and in patients with MI and acute coronary syndromes has been shown to reduce the composite endpoint of death, reinfarction, and the need to revascularize the target lesion at follow-up.
  • The current guidelines recommend the use of a IIb/IIIa inhibitor for patients in whom PCI is planned. For high-risk patients with NSTEMI who do not undergo PCI, a IIb/IIIa inhibitor may be used for 48 to 72 hours (Table 5).

Table 5: Glycoprotein IIb/IIIa Inhibitors

Agent Loading Dose (IV) Maintenance Dose (IV) Duration of Infusion FDA Approved Indications
Abciximab 0.25 mg/kg 0.125 µg/kg/min
max 10 µg/min
12-24 hr Coronary intervention
Eptifibatide 180 µg/kg 2 µg/kg/min Up to 72 hr Acute coronary syndrome
Coronary intervention
Tirofiban 0.4 µg/kg/min for 30 min 0.1 µg/kg/min 12-24 hr Acute coronary syndrome
Coronary intervention
  • The evidence is less well established for the direct thrombin inhibitor, bivalirudin. The 2007 American College of Cardiology (ACC) and the American Heart Association (AHA) guidelines recommend bivalirudin as an alternative to heparin therapy for patients who cannot receive heparin for a variety of reasons (e.g., heparin-induced thrombocytopenia).

Statin Therapy

  • A statin should be started in all patients with myocardial infarction without known intolerance or adverse reaction prior to hospital discharge. Preferably, a statin would be started as soon as a patient is stabilized after the presentation.
  • The Pravastatin or Atorvastatin Evaluation and Infection—Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) trial suggested a benefit of starting patients on high-dose therapy from the start (e.g., atorvastatin 80 mg/day).

Aldosterone Antagonists

  • In the Epleronone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) trial, a mortality benefit was seen with eplerenone administration in all post-MI patients, provided multiple criteria were met.
  • The criteria included concomitant use of an ACE inhibitor, ejection fraction less than 40%, symptomatic heart failure or diabetes, a creatinine clearance greater than 30 mL/min, and a potassium level less than 5 mEq/dL. In patients that meet these criteria, the use of eplerenone has a Class I indication.

Surgical Treatments

  • Percutaneous coronary intervention (PCI). In primary PCI, the doctor performs a coronary angiogram (injecting dye into the arteries) to see where the artery is blocked. The doctor then performs balloon angioplasty (widening an artery with a balloon), often with stent placement, to keep the artery open.

Primary PCI

image080

rx
www.rxharun.com
  • PCI (or percutaneous transluminal coronary angioplasty – PTCA) is regarded as superior to fibrinolysis in the management of AMI and is becoming increasingly available for initial patient care.
  • Primary angioplasty provides an early assessment of the extent of the underlying disease.
  • Any delay in primary PCI after a patient arrives at hospital is associated with higher mortality in hospital. Time to treatment should therefore be as short as possible. Door (or diagnosis) to treatment time should be less than 90 minutes, or less than 60 minutes if the hospital is PCI ready and symptoms started within 120 minutes.
  • There is general agreement that PCI should be considered if there is an ST-elevation ACS, if symptoms started up to 12 hours previously. There is no consensus whether PCI is also beneficial in patients presenting more than 12 hours from the onset of symptoms in the absence of clinical and/or ECG evidence of ongoing ischaemia.
  • Patients should receive a glycoprotein IIb/IIIa inhibitor to reduce the risk of immediate vascular occlusion and should also receive either unfractionated heparin, a low molecular weight heparin (eg, enoxaparin), or bivalirudin.
  • Prasugrel in combination with aspirin is recommended as an option for preventing atherothrombotic events in adults with unstable angina, non-ST-elevation myocardial infarction (NSTEMI) or ST-elevation myocardial infarction (STEMI) having primary or delayed PCI.
  • Balloon angioplasty following myocardial infarction reduces death, non-fatal myocardial infarction, and stroke compared with thrombolytic reperfusion. However, up to 50% of patients experience re-stenosis and 3-5% recurrent myocardial infarction.
  • There is no evidence to suggest that primary stenting reduces mortality when compared with balloon angioplasty but stenting seems to be associated with a reduced risk of re-infarction and target vessel revascularisation.
  • NICE, therefore, recommends that intracoronary stent implantation should be used in patients undergoing primary PCI.

Facilitated PCI

  • Facilitated PCI is the use of pharmacological reperfusion treatment delivered prior to a planned PCI.
  • There is no evidence of a significant clinical benefit and so facilitated PCI is currently not recommended.

Rescue PCI

  • Rescue PCI is defined as PCI performed on a coronary artery which remains occluded despite fibrinolytic therapy.
  • Rescue PCI is associated with a significant reduction in heart failure and re-infarction and a lower all-cause mortality and so should be considered when there is evidence of failed fibrinolysis based on clinical signs and insufficient ST-segment resolution, if there is clinical or ECG evidence of a large infarct and if the procedure can be performed less than 12 hours after the onset of symptoms.

Fibrinolytic drugs

For patients who cannot be offered PCI within 90 minutes of diagnosis, a thrombolytic drug should be administered along with either unfractionated heparin (for maximum two days), a low molecular weight heparin (eg, enoxaparin) or fondaparinux. Thrombolytic drugs break down the thrombus so that the blood flow to the heart muscle can be restored to prevent further damage and assist healing.

Reperfusion by thrombolysis is often gradual and incomplete and may be inadequate. There is a risk of early or late reocclusion and a 1-2% risk of intracranial hemorrhage.

  • Fibrinolytic drugs act as thrombolytics by activating plasminogen to form plasmin, which degrades fibrin and so breaks up the thrombi.
  • Streptokinase and alteplase have been shown to reduce mortality. Reteplase and tenecteplase are also licensed for AMI.
  • Streptokinase and alteplase are given by intravenous infusion. Reteplase and tenecteplase can be given by rapid bolus injection.
  • The benefit is greatest in those with ECG changes that include ST-segment elevation (especially in those with anterior infarction) and in patients with bundle branch block.
  • The earlier the treatment is given, the greater the absolute benefit. Alteplase, reteplase, and streptokinase need to be given within 12 hours of symptom onset, ideally within one hour. Tenecteplase should be given as early as possible and usually within six hours of symptom onset.
  • Bleeding complications are the main risks associated with thrombolysis. Contra-indications for thrombolysis include patients with bleeding disorders, or a history of recent haemorrhage, trauma, surgery or acute cerebrovascular event.
  • Persistence of antibodies to streptokinase can reduce the effectiveness of subsequent treatment and so streptokinase should not be used again after the first administration.

Antithrombotic therapy without reperfusion therapy

  • In patients presenting within 12 hours after the onset of symptoms but reperfusion therapy is not given, or in patients presenting after 12 hours, aspirin, clopidogrel and an antithrombin agent (heparin, enoxaparin or fondaparinux) should be given as soon as possible.
  • For patients who do not receive reperfusion therapy, angiography before hospital discharge is recommended (as for patients after successful fibrinolysis) if no contraindications are present.

Coronary bypass surgery

Only a few patients need a coronary artery bypass graft (CABG) in the acute phase but CABG may be indicated:

  • After failed PCI, coronary occlusion not amenable for PCI, or the presence of refractory symptoms after PCI.
  • Cardiogenic shock, or mechanical complications – eg, ventricular rupture, acute mitral regurgitation, or ventricular septal defect.
  • Multivessel disease.
  • In patients with a non-emergency indication for CABG (eg, multisystem disease), it is recommended to treat the infarct-related lesion by PCI and to perform CABG later in more stable conditions if possible.

Coronary artery bypass graft (CABG)

  • This surgery bypasses the blocked arteries by using a graft of another blood vessel (usually from your arm or leg) to restore blood flow to the heart.

Nutrition and Dietary Supplements

  • Healthy eating habits can help reduce high cholesterol, high blood pressure, and excess weight, three of the major risk factors for heart disease. The American Heart Association (AHA) has developed dietary guidelines that help lower fat and cholesterol intake and reduce the risk of heart disease and heart attack. The AHA does not recommend very low fat diets, because new research shows that “good” fats, such as those found in olive oil and avocadoes, are good for your heart.
  • Fad diets are popular, but they may not help you lose weight and keep it off. In some cases, they may not even be healthy. Any healthy diet will include a variety of foods. If a diet bans an entire food group (such as carbohydrates), it is probably not healthy.

The AHA recommends the following for healthy eating:

  • Grains: 6 to 8 servings per day (half of those servings should be whole grains)
  • Vegetables: 3 to 5 servings per day
  • Fruits: 4 to 5 servings per day
  • Fat-free or low-fat dairy: 2 to 3 servings per day
  • Lean meat, poultry, and seafood: 3 to 6 oz. per day (about the size of a deck of cards)
  • Fats and oils: 2 to 3 tbsp. per day (use unsaturated fats such as olive oil or canola oil)
  • Nuts, seeds, legumes: 3 to 5 servings per week
  • Sweets, sugars: 5 or fewer servings per week (the fewer, the better)

In addition, the AHA also recommends eating 2 servings of fatty fish (such as salmon or lake trout) per week; holding sodium (salt, including salt already added to food) to 2,400 mg per day or less; and limiting alcohol intake to one drink a day for women and two for men.

Diets for People with High Blood Pressure

  • People with high blood pressure especially need to lower the amount of sodium in their diet. The DASH diet (Dietary Approaches to Stop Hypertension) emphasizes a diet rich in fruits, vegetables, and low-fat or nonfat dairy products that provide high intake of potassium, magnesium, and calcium sources.
  • Sodium intake should be between 1,500 to 2,400 mg per day (the lower, the better). Weight loss, regular exercise, and limiting alcohol are also very important factors for lowering blood pressure.

Mediterranean Diet

  • The Mediterranean Style Diet concentrates on whole grains, fresh fruits and vegetables, fish, olive oil, and moderate wine consumption. The Mediterranean Style Diet is not low fat; it is low in saturated fat, but high in monounsaturated fat.
  • It appears to be heart healthy – In a long-term study of 423 people who had a heart attack, those who followed a Mediterranean Style Diet had a 50 to 70% lower risk of recurrent heart disease compared with people who received no special dietary counseling.

Vitamins and Supplements

  • Some supplements –  may help lower your risk factors for heart attacks, such as high blood pressure or high cholesterol. Most do not work as well as prescription medications. But some can be used along with prescription medications in your treatment. If you have had a heart attack, or are at high risk of having one, ask your doctor before taking any supplements. Your physician should manage your heart disease, and you should not take supplements without your physician’s approval. Many supplements can have negative interactions with medications used to treat heart disease.
  • B vitamins – Folic acid, vitamin B6, and vitamin B12 help the body break down homocysteine, an amino acid that has been linked to increased risk of heart disease and stroke. Researchers believe that homocysteine may also contribute to atherosclerosis by damaging artery walls, making it easier for blood clots to form, but so far they haven’t found a definite link. Researchers also do not yet know whether taking B vitamins reduces the risk of atherosclerosis or heart attack, nor do they know how much might have an effect. Talk to your doctor about checking your homocysteine levels and whether you should take a B complex vitamin supplement. In the meantime, be sure to get enough B vitamins through your diet by eating fruits and leafy green vegetables every day.
  • Vitamin D – Studies show that lower levels of vitamin D are associated with higher risk of myocardial infarction and premature death. Dose recommendations for vitamin D vary greatly between physicians. Your physician may do blood work to monitor your vitamin D levels and determine the appropriate dose for your needs.
  • Omega-3 fatty acids – There is good evidence that omega-3 fatty acids (known as EPA and DHA) found in fish oil can help treat atherosclerosis by preventing the development of plaque and blood clots. Omega-3s can also help prevent heart disease, lower blood pressure, and reduce the level of triglycerides (fats) in the blood. The AHA recommends that people eat at least 2 servings of fatty fish (such as salmon) per week. For people who have had a heart attack, several studies show that eating fish or taking fish oil reduces the risk of both fatal and nonfatal heart attacks, as well as lowers your risk of death from any cause. Because fish oil at high doses can increase the risk of bleeding, talk to your doctor before taking a high dose (more than 1 g per day), especially if you already take blood-thinning medication.
  • Beta-sitosterol – A plant sterol, a chemical found in plants that can stop cholesterol from being absorbed by the intestines. A number of well-designed scientific studies have shown that beta-sitosterol does lower LDL (bad) cholesterol levels in the body. Beta-sitosterol may lower the amount of vitamin E and beta-carotene absorbed by the body, so you may want to ask your doctor if you need to take extra E or carotene.
  • Policosanol – A mix of waxy alcohols usually derived from sugar cane and yams. Several studies have indicated it may lower LDL (bad) cholesterol and possibly even raise HDL (good) cholesterol. One study found that policosanol was equivalent to fluvastatin (Lescol) and simvastatin (Zocor) in lowering cholesterol levels. It may also help stop blood clots from forming. However, almost all the studies have been conducted in Cuba by a research group that uses a proprietary form of policosanol and is funded by the manufacturer. So it is hard to evaluate the evidence. Policosanol may increase the risk of bleeding, and it should not be taken by people who also take blood-thinning medications.
  • Coenzyme Q10 (CoQ10) – Researchers believe that CoQ10 may help stop blood clots from forming and boost levels of antioxidants. One study found that people who received daily CoQ10 supplements within 3 days of a heart attack were much less likely to experience another heart attack and chest pain. They were also less likely to die from heart disease than those who did not receive the supplements. Statins, drugs that lower cholesterol, can actually interfere with the body’s natural ability to make CoQ10, so your doctor may recommend taking a CoQ10 supplement. Still, more research is needed to say whether CoQ10 has any role in preventing or treating atherosclerosis. CoQ10 may interact with blood-thinning medications, such as warfarin (Coumadin), and others since CoQ10 helps blood clot it may make these medications less effective.
  • Psyllium – This fiber helps lower cholesterol levels and blood sugar levels. If you take medicine for diabetes or have digestive problems, talk to your health care provider before taking psyllium. Always take your medications at least a few hours away fro when you take psyllium.
  • L-carnitine – Studies suggest that people who take L-carnitine (an amino acid) soon after a heart attack may be less likely to have a subsequent heart attack, die of heart disease, experience chest pain and abnormal heart rhythms, or develop heart failure. (Heart failure occurs when the heart can’t pump blood properly and blood backs up into the lungs and legs.) Studies also suggest that people with heart disease who take carnitine may be better able to exercise. Most studies used a special form of carnitine called propionyl-L-carnitine. L-carnitine can interact with certain medications, including thyroid and blood-thinning medications such as warfarin (Coumadin). Talk to your provider about whether L-carnitine is right for you.

Herbal Remedies

Herbs should not be used in place of emergency medical attention for a heart attack, nor should they be used by themselves to lower your risk of heart attack after you have had one. However, certain herbs can be used along with prescription medications in your treatment, although many can interact with a variety of medications. The herbs below have the potential to interact with several different medications. It is critical that you consult your physician before adding any herbs to your regimen. If you have had a heart attack, or are at high risk of having one, ask your doctor before taking any herbs.

  • Hawthorn (Cras monogynataegu) – Hawthorn contains the polyphenols rutin and quercetin, and was used traditionally to treat cardiovascular diseases. Animal and laboratory studies show that hawthorn has antioxidant properties that help protect against the formation of plaques and may help lower high cholesterol and high blood pressure. Talk to your doctor before taking hawthorn, as it can interact with other drugs taken for heart disease and high blood pressure.
  • Garlic (Allium sativum) – Studies show that fresh garlic and garlic supplements may lower cholesterol levels, prevent blood clots, and destroy plaque. However, other studies show mixed evidence. In one study, people who had a previous heart attack and then took a garlic oil extract for 3 years had fewer second heart attacks and a 50% reduction in death rate than those who did not take garlic. Garlic can increase the risk of bleeding. Garlic can interact with a number of medications, including some of those used to treat HIV/AIDS. You should not take garlic if you are also taking blood-thinning medication.
  • Bilberry (Vaccinium myrtillus) – and other flavonoids. A close relative of the cranberry, bilberry fruits contain flavonoid compounds called anthocyanidins. Flavonoids are plant pigments that have antioxidant properties. Researchers think they may help prevent several illnesses, including heart disease and diabetes. Bilberry has been used traditionally to treat heart disease. But only animal and test tube studies have been done. Animal studies have found that anthocyanidins and other flavonoids may strengthen blood vessels, improve circulation, and prevent LDL (bad) cholesterol from being damaged (which may cause blood clots to form in arteries). Bilberry may have a blood-thinning effect and therefore can increase the risk of bleeding in people taking blood-thinning medications such as warfarin (Coumadin) and others. Talk to your health care provider.
  • Green tea (Camellia sinensis) – Population studies suggest that regularly drinking green tea may reduce the risk of heart attack from atherosclerosis. It also may help you lower lose weight and your cholesterol levels. More research is needed to know for sure. Avoid caffeinated varieties.
  • Kudzu (Pueraria lobata) – Kudzu has been used traditionally to treat heart disease, including heart attack and congestive heart failure. A few studies suggest it may help relieve angina, but the studies were of poor quality. More research is needed to know whether kudzu has any benefit for heart disease. Kudzu might slow blood clotting, so people with bleeding disorders or who take blood-thinning medications, such as warfarin (Coumadin), should use caution. Talk to your doctor.

Homeopathy

  • Homeopathy should not be used instead of immediate medical attention for a heart attack. However, homeopathy may be used to help reduce the risk of heart disease. Although few studies have examined the effectiveness of specific homeopathic remedies, professional homeopaths would recommend appropriate therapy to lower high blood pressure and cholesterol.
  • Before prescribing a remedy, homeopaths take into account your constitutional type. In homeopathic terms, a person’s constitution is their physical, emotional, and intellectual makeup. An experienced homeopath assesses all of these factors when determining the most appropriate remedy for you as an individual.

Acupuncture

  • Acupuncture may be helpful in reducing some risk factors for heart disease. Some studies show that it can help people who want to stop smoking, and it may help some people lose weight and lower their blood pressure.

Massage and Physical Therapy

  • Although few studies have examined the effectiveness of massage therapy for heart disease, massage has a relaxing effect and can reduce stress-related hormone levels. Lowering stress hormone levels can lower cholesterol and blood pressure, reducing your risk of heart disease.
  • In addition, relaxation techniques may help you make lifestyle changes such as eating healthy, quitting smoking and exercising. At least one study found that massage can lower blood pressure.

Prevention

Risk factors for heart attack include cigarette smoking, high blood pressure, high blood cholesterol levels, diabetes, excess weight, lack of physical exercise, and a family history of heart disease. Hence, the following lifestyle changes can help to prevent a heart attack occurring as well as recovery from a heart attack:

  • stop smoking and avoid second-hand smoke
  • control high blood pressure or high blood cholesterol levels
  • get regular medical check-ups and take medication as prescribed
  • exercise regularly, especially healthy heart exercise
  • maintain a healthy weight
  • eat a healthy heart diet
  • manage diabetes
  • avoid drinking alcohol or do so in moderation.

Additionally, ‘blood-thinning’ medications, beta blockers, ACE inhibitors, and cholesterol-lowering drugs may be prescribed long-term to reduce the risk of a future heart attack.

Other statistics from the American Heart Association:

  • Over 500,000 American women die of cardiovascular disease each year. This twice the number of deaths from all cancers combined (lung cancer, the leading cause of cancer deaths, claims approximately 65,000 deaths per year, and breast cancer kills around 40,000 women per year).
  • One in three women have some form of cardiovascular disease.
  • 38% of women who have heart attacks die within the first year compared to 25% of men.
  • 35% of women have a second heart attack within six years of the first attack compared to 18% of men.
  • Over 60,000 women die of stroke each year; approximately 60% of stroke deaths occur in women.

Reference

Magnesium Deficiency

Print Friendly, PDF & Email

Sharing to Spread to the World

92 thoughts on “Myocardial Infarction; Causes, Symptoms, Diagnosis, Treatment”

Leave a Reply

Your email address will not be published.