Overview of myocardial infarction
Myocardial infarction (MI) or heart attack is a medical emergency condition in which the blood supply to the heart suddenly reduces or stops, causing the myocardium to die from lack of oxygen (myocardial ischemia).
Myocardial infarction is the most dominant manifestation of ischemic heart diseases (IHDs).1 Although it may be a minor event in a lifelong chronic disease and remains undetected, myocardial infarction frequently leads to sudden death in both men and women all over the world.
Approximately one-third of individuals die of cardiovascular diseases (CVDs) globally and 80% of these deaths occur in developing countries.2 In India, the deaths due to CVDs are expected to increase from 1.17 million in 1990 and 1.59 million in 2000 to 2.03 million by the year 2010.3
A definite diagnosis of myocardial infarction can be made in patients who have a number of atherosclerotic risk factors along with the presence of symptoms consistent with myocardial ischemia. The goals of the therapy in myocardial infarction are immediate restoration of normal coronary blood flow and maximum salvage of functional myocardium. These therapeutic goals can be achieved through appropriate and timely medical interventions.
Pathophysiology and Risk Factors for myocardial infarction
The commonest cause of myocardial infarction is rupture of an atherosclerotic plaque within a coronary artery followed by arterial spasm and subsequent thrombus formation. The severity of an myocardial infarction depends on the level and duration of the arterial occlusion. More the proximal coronary occlusion, the greater is the chance of death due to a mechanical complication. When the duration of the occlusion is prolonged, there are more chances of irreversible myocardial damage distal to the occlusion.
Risk factors involved in the formation of atherosclerotic plaque are as follows:
- Increasing age
- Male gender
- Diabetes mellitus
- Poorly controlled hypertension
- Family history of IHDs
- Sedentary lifestyle
- Psychosocial stress
Other risk factors (nonatherosclerotic) which cause myocardial infarction include the following:
- Vasculitis (inflammation of blood vessels)
- Coronary vasospasm
- Coronary emboli
- Coronary anomalies
- Hypoxia due to carbon monoxide poisoning or acute pulmonary disorders
- Use of drugs such as cocaine, amphetamines and ephedrine
Clinical Features (Symptoms of myocardial infarction)
The most common symptom of acute myocardial infarction is chest pain, which is similar to angina but usually more severe, persists for longer duration and not relieved by taking rest or consuming sublingual nitrates. The pain is described as a sensation of tightness, pressure or squeezing. It lasts for more than 20 min and usually radiates to the left arm, neck, jaw, back and mid-upper abdomen, where it may mimic heartburn.
Other associated symptoms include
- Sudden profuse sweating
- Nausea with or without vomiting
- Shortness of breath
- Anxiety and a sense of impending doom
Elderly patients with myocardial infarction often present with shortness of breath or faintness as their main complaint. They may also present with only altered mental status. Myocardial infarction may occur with atypical symptoms or even without symptoms, which may be detected only through further investigations.2
Diagnosis of myocardial infarction
The definite diagnosis of acute myocardial infarction is based on the WHO criteria, which requires either defined electrocardiography (ECG) changes or ischemic symptoms and presence of cardiac biomarkers (preferably troponin).4 Several radionuclide techniques have also been utilized to detect the presence of acute myocardial infarction.
Electrocardiography is an essential part of the diagnostic work-up of patients suspected with MI.5 Changes in the ST-T waveforms and the Q-waves, when present, suggest the infarct-related artery and allow estimation of the amount of myocardium at risk. However, an ECG alone is insufficient to diagnose acute myocardial infarction as the above changes may also be seen in conditions such as acute left ventricular hypertrophy or pericarditis (inflammation of the fibrous sac surrounding the myocardium). As mistakes in the interpretation of myocardial infarction are relatively common, the failure to identify high-risk features will have an unfavorable impact on the quality of patient care.6
Cardiac markers are proteins from myocardial tissue found in the blood. Injury to the myocardial cells results in the release of intracellular enzymes into the blood, thereby allowing their detection by blood tests. Earlier, the serum cardiac marker creatine kinase (CK) and an isoenzyme, creatine kinase-myocardial band (CK-MB) were used to diagnose myocardial infarction in its earliest stages.
Current guidelines favors the detection of troponin subunits I or T, which are very myocardial specific and can be detected early in the blood before permanent myocardial injury develops.7 Raised troponins level in a patient with chest pain may accurately predict a high likelihood of a myocardial infarction. Troponins will begin to increase within 3–12 h following MI and remain elevated up to 5–9 days for troponin I and up to 2 weeks for troponin T.
An echocardiogram may be performed in order to compare areas of the lower left side of the heart (ventricle) that are contracting normally with those that are not. Most patients with acute myocardial infarction have regional wall motion abnormalities readily seen on ECG.
Echocardiography for diagnosis of myocardial infarction is most helpful in patients with a high clinical suspicion but have a normal or nondiagnostic ECG and atypical symptoms.8 In patients with symptoms and ECG evidence indicating typical of myocardial infarction, treatment should not be delayed by waiting for an echocardiogram to be performed. Further, the wall motion abnormalities are not specific for myocardial infarction and may be caused by ischemia or prior infarction.
The use of myocardial perfusion or myocardial viability studies is necessary for the evaluation of acute myocardial infarction in any of the following circumstances:
- Emergency assessment of myocardial risk in patients with possible acute myocardial infarction when ECG and cardiac enzymes are nondiagnostic.
- Post-MI, in order to assess extent of stress-induced ischemia.
- Post-MI, in order to detect infarct size or assess myocardium at risk.
- Post-MI, in order to assess areas of cardiac viability.
Treatment of myocardial infarction
Emergency First-Line Therapy
The basic goal in the management of acute phase of myocardial infarction is to salvage as much areas of myocardium as possible and to prevent further complications.
In addition to routine therapy such as bed rest, oxygen (when needed) and continuous cardiac monitoring, the 2002 ACC/AHA guidelines recommend the following therapies to all patients with probable myocardial infarction:9
Nitrates: Initially given sublingually, followed by intravenous administration for the relief of ischemia and associated symptoms.
Morphine: The preferred pain relief drug due to its ability to dilate blood vessels to the heart in addition to its pain relief properties.
Antiplatelet agents: Aspirin should be administered immediately. Aspirin has been shown to decrease the mortality and reinfarction rates after myocardial infarction. Clopidogrel can be used in case of aspirin allergy.
Beta-blockers: When not contraindicated, beta-blockers such as metoprolol or atenolol are used for heart rate control and subsequent decrease of myocardial oxygen demand. Beta-blockers also reduce the rates of reinfarction and recurrent ischemia.
Calcium-channel blockers: Agents such as verapamil or diltiazem are recommended in patients with recurring ischemia when beta-blockers are contraindicated and in absence of left ventricular dysfunction or other contraindication to their use.
Antithrombin agents: Thrombolytic therapy administered within the first 2 h can occasionally abort myocardial infarction and significantly reduce the mortality rate.
Patients with ST-segment elevation myocardial infarction (STEMI) are presumed to have an occlusive thrombosis in an epicardial coronary artery. Therefore, they are suitable for immediate reperfusion, either with thrombolytic therapy, percutaneous coronary intervention (PCI) or coronary artery bypass surgery. In non-ST-segment elevation myocardial infarction (NSTEMI), there is a sudden narrowing of a coronary artery with preserved but reduced flow to the distal myocardium. Therefore, anticoagulation and antiplatelet agents are given to prevent the occlusion of the narrowed artery.
Although pharmacological thrombolysis restores coronary artery patency in about two-thirds of myocardial infarction patients, mechanical reperfusion with primary angioplasty (widening of a narrowed or totally obstructed artery) and stenting (implantation of thin metal scaffolding into a narrowed coronary artery) has higher patency rates with fewer complications, especially in high-risk patients.10
The outcome of primary angioplasty can be improved with adjunctive pharmacotherapy and new device technology such as use of drug-eluting stents. These are stents that slowly release drugs in order to prevent scar tissue from forming inside the stent.
Complications of myocardial infarction
Some possible complications that may occur after an myocardial infarction include the following:
- Myocardial rupture.
- Congestive heart failure: A condition that impairs the ability of the heart to pump sufficient blood through the body.
- Arrhythmias: Abnormal heart rhythms.
- Cardiogenic shock: A state of inadequate tissue perfusion due to cardiac dysfunction.
Life after Heart Attack
Cardiac rehabilitation is the process by which a myocardial infarction patient or a patient with IHD is encouraged to achieve their full potential in terms of physical and psychological health. Cardiac rehabilitation includes a program of structured exercise, which improves morbidity and reduces mortality in myocardial infarction patients. Other rehabilitation programs are general health education and information on stress management.
Risk-factor modification is an important aspect in the reduction and alleviation of myocardial ischemia. Indeed, use of medical therapy in controlling the risk factor may reduce the risk of future cardiac events to a greater degree than revascularization strategies.
Secondary prevention of CVDs includes general measures and specific drug therapy, according to the individual risk pattern. Among the general measures, cessation of smoking is most important, followed by daily exercise (avoid exerting activities), maintenance of optimal body weight and a healthy diet. In most cases, secondary prevention also includes specific drug therapies. Aspirin, statins, beta-blockers and ACE (angiotensin-converting enzyme) inhibitors are the cornerstones of this drug therapy.
You May Also Like To Read
1. de Torbal A, Boersma E, Kors JA, van Herpen G, Deckers JW, van der Kuip DA, et al. Incidence of recognized and unrecognized myocardial infarction in men and women aged 55 and older: The Rotterdam Study. Eur Heart J. 2006; 27(6): 729–736.
2. Thygesen K, Alpert JS, White HD. Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. J Am Coll Cardiol. 2007; 50(22): 2173–2195.
3. Ghaffar A, Reddy KS, Singhi M. Burden of non-communicable diseases in South Asia. BMJ. 2004; 328: 807–810.
4. Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined - a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000; 36(3): 959–969.
5. Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LE, Hand M, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines 2004. J Am Coll Cardiol. 2004; 44: 671–719.
6. Masoudi FA, Magid DJ, Vinson DR, Tricomi AJ, Lyons EE, Crounse L, et al. Implications of the failure to identify high-risk electrocardiogram findings for the quality of care of patients with acute myocardial infarction. Circulation. 2006; 114: 1565–1571.
7. Eisenman A. Troponin assays for the diagnosis of myocardial infarction and acute coronary syndrome: Where do we stand? Expert Rev Cardiovasc Ther. 2006; 4(4): 509–514.
8. Role of echocardiography in acute coronary syndromes. Sally C Greaves. Heart. 2002; 88(4): 419–425.
9. Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, et al. ACC/AHA 2002 guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction—summary article: A report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on the Management of Patients With Unstable Angina). J Am Coll Cardiol. 2002; 40: 1366–1374.
10. Katritsis D, Karvouni E, Webb-Peploe MM. Reperfusion in acute myocardial infarction: Current concepts. Prog Cardiovasc Dis. 2003; 45(6): 481–492.
Written by: healthplus24.com team
Date last updated: February 01, 2015