Sutha's Blog

Pathophysiology of myocardial infarction

The spectrum of myocardial injury depends not only on the intensity of impaired myocardial perfusion but also on the duration and the level of metabolic demand at the time of the event. The damage in the myocardium is essentially the result of a tissue response that includes apoptosis (cell death) and inflammatory changes. Therefore, the hearts of patients who suddenly die from an acute coronary event may show little or no evidence of damage response to the myocardium at autopsy.

The typical myocardial infarction initially manifests as coagulation necrosis that is ultimately followed by myocardial fibrosis. Contraction-band necrosis is also seen in many patients with ischemia. This is followed by reperfusion, or it is accompanied by massive adrenergic stimulation, often with concomitant myocytolysis.

The left coronary artery system covers more territory than does the right system; therefore, a myocardial infarction in this system is most likely to produce extensive injury, with impairment of function, pulmonary congestion, and low output. Occlusion of the left coronary artery may also cause a left anterior hemiblock or a left posterosuperior hemiblock conduction abnormality; these effects are evidenced by a change of frontal axis on the electrocardiogram (ECG). (See Electrocardiogram.)

Inferior-wall myocardial infarction and right ventricular myocardial infarction

In severe cases of acute inferior-wall myocardial infarction with RV involvement, the forward delivery of blood from the RV to the LV may be insufficient to fill the LV, resulting in low blood pressure even if the LV is intact. (See Physical Examination.)

Chemoreceptor activation in the myocardium actuates vagal (parasympathetic) efferent discharge, known as the Bezold-Jarisch reflex, which causes bradycardia and vessel dilation that may further lower blood pressure. Adenosine may accumulate in the infarct zone secondary to a local inhibition of adenosine deaminase, for which aminophylline may act pharmacologically as an antagonist. The hemodynamic changes resemble many of those seen with pericardial constriction or tamponade. Patients with this condition respond well to an infusion of normal sodium chloride solution. Improvement with such infusion compensates for failure of the pumping action of the RV; it reduces vagal tone, and it deactivates the pressure sensors that were sending a hormonal signal to the kidneys to retain salt.

Arrhythmogenesis

In addition to the direct effects of ischemia and tissue hypoxia, decreased removal of noxious metabolites, including potassium, calcium, amphophilic lipids, and oxygen-centered free radicals, also impair ventricular performance. These abnormalities promote potentially lethal arrhythmias.

Pericarditis

Epicardial inflammation may initiate pericarditis, which is seen in more than 20% of patients presenting with Q-wave infarctions.

Reduced systolic function

Lack of adequate oxygen and insufficient metabolite delivery to the myocardium diminish the force of muscular contraction and decrease systolic wall motion in the affected territory.

Abnormal regional wall motion

Even brief deprivation of oxygen and the requisite metabolites to the myocardium diminishes diastolic relaxation and causes abnormal regional systolic contractile function, wall thickening, and abnormal wall motion. If the area affected is extensive, diminished stroke volume and cardiac output may result.

Hypokinesis and akinesis

In general, regions of hypokinesis and akinesis of the ventricular myocardium reflect the location and extent of myocardial injury.

Myocardial infarction expansion

In general, expansion of infarcted myocardium and resultant ventricular dilatation (ie, ventricular remodeling) ensues within a few hours after the onset of a myocardial infarction. An expanding myocardial infarction leads to thinning of the infarct zone and realignment of layers of tissue in and adjacent to it, causing ventricular dilatation.

Myocardial rupture

Myocardial rupture was seen in as many as 10% of fatal myocardial infarctions before the era of thrombolytics, but it is now encountered much less often. When rupture occurs, it may be associated with large infarctions; indications include cardiogenic shock or hemodynamically significant arrhythmia. Patients may have a history of hypertension with ventricular hypertrophy.

Ventricular aneurysm

A ventricular aneurysm is an outward bulging of a noncontracting segment. In the early days of cardiac imaging, ventricular aneurysms were seen in as many as 20% of patients with Q-wave myocardial infarction, but now it is seen in less than 8%.

Cardiogenic shock

In patients with extensive myocardial injury, coronary blood flow diminishes as cardiac output declines and heart rate accelerates. Because coronary artery disease is usually generalized or diffuse, ischemia that occurs at a distance from the infracted segment may result in a vicious cycle in which a stuttering and expanding myocardial infarction ultimately leads to profound LV failure, hypotension, and cardiogenic shock.

Effect on diastolic function

Immediately after the onset of myocardial infarction, the ability of ischemic myocardium to relax declines. Relaxation is an active process that uses ATP. Impaired relaxation increases LV end-diastolic volume (LVEDV) and LV end-diastolic pressure (LVEDP).

The increased LVEDP results in ventricular dilation, increased pulmonary venous pressure, decreased pulmonary compliance, and interstitial and (ultimately) alveolar pulmonary edema. These effects lead to increased hypoxemia, which may worsen ischemic injury to the myocardium.

Next Section: Eti

Anotomy of the heart

The right and left coronary arteries most often arise independently from individual ostia in association with the right and left aortic valve cusps.

The left anterior descending (LAD) and left circumflex (LCX) coronary arteries arise at the left main coronary artery bifurcation; they supply the anterior LV, the bulk of the interventricular septum (anterior two thirds), the apex, and the lateral and posterior LV walls. The right coronary artery (RCA) generally supplies the right ventricle (RV), the posterior third of the interventricular septum, the inferior wall (diaphragmatic surface) of the left ventricle (LV), and a portion of the posterior wall of the LV (by means of the posterior descending branch).

When the posterior descending coronary artery (PDA), which supplies the posterior interventricular septum, arises from the LCX artery, the circulation is called left dominant. Most often, the PDA arises from the RCA; this anatomy is called right-dominant circulation.

In two thirds of patients, the first branch of the RCA is the conus artery, which supplies the conus arteriosus (RV outflow tract); occasionally the conus arteriosus arises from a separate orifice.

In 60% of patients, the sinus node artery arises from the proximal RCA, and in 40% of patients, it arises from the LCX artery. The anterior branches supply the free wall of the RV, and the acute marginal branches supply the RV. When the RCA extends to the crux (the origin of the PDA), it supplies the atrioventricular (AV) node (90%); otherwise, the AV node is supplied by the LCX.

Therefore, obstruction of the RCA commonly affects the sinus node and the AV node, resulting in bradycardia, with or without heart block. Not surprisingly, RCA occlusion frequently manifests with sinus bradycardia, AV block, RV myocardial infarction, and/or inferoposterior myocardial infarction (of the LV). (See Eti