PATHOPHYSIOLOGY OF CORONARY ARTERY DISEASE

ETIOLOGY AND PATHOPHYSIOLOGY:

In greater than 90% of patients with AMI, a blood clot formed sharply, often associated with plaque rupture, occludes the artery (which was previously partially blocked by atherosclerotic plaque), which provides blood to the area damaged. Impaired platelet function induced by alterations in the endothelium of atherosclerotic plaque presumably contributes to the genesis of the thrombus. A spontaneous thrombolysis occurs in about 2 / 3 of patients, so that, after 24 h, thrombotic occlusion is found only in 30% of cases.

 

The IMA is rarely caused by arterial embolism (eg. In the aortic or mitral stenosis, infective endocarditis and endocarditis arrowroot). Cocaine causes a major coronary spasm and individuals who use it may develop angina or AMI induced by cocaine. Angiographic and autopsy studies have shown that cocaine-induced coronary thrombosis may occur on normal coronary arteries or duplicate an existing atheroma.

The IMA is mainly a disease of the VS, although the damage could extend to the right ventricle (RV) or the atria. RV infarction is usually the result of occlusion of right coronary artery or a dominant circumflex artery and is characterized by a high pressure filling of the RV, often with severe tricuspid regurgitation and reduced cardiac output. A degree of RV dysfunction occurs in about half of patients with infero-posterior infarction and causes hemodynamic instability in 10-15% of cases. RV dysfunction should be considered in every patient with acute infero-posterior and elevated jugular venous pressure and hypotension or shock.

 

The heart's ability to continue to maintain the pump function is directly proportional to the size of myocardial injury. The patient died of cardiogenic shock usually have a heart attack, or a combination of myocardial scar and again, which affects 50% of the mass of VS. The earlier heart attacks tend to be larger and have a worse prognosis than the inferior-posterior infarction. They are usually caused by occlusion of the left coronary branches, especially the left anterior descending artery, and inferior-posterior infarcts reflect right coronary artery or occlusion of a dominant circumflex artery.

Transmural infarcts affecting the myocardial wall thickness at all, dall'epicardio endocardium, and is usually characterized by pathological Q wave ECG. The non-transmural or subendocardial infarcts do not extend throughout the ventricular wall and cause only ST-segment abnormalities and T wave Subendocardial infarcts usually involve the inner third of the myocardium, where wall tension is highest and the myocardial blood flow is more vulnerable to circulatory changes. They may also follow prolonged hypotension from any cause. Since the extent of myocardial necrosis through the wall can not be precisely determined clinically, infarcts are more correctly classified as non-Q and Q according to the ECG. The amount of necrotic myocardium can be estimated from the volume and duration of the increase in CK.

SIGNS AND SYMPTOMS:

 

About 2 / 3 of patients experience warning symptoms a few days or weeks before the event, including unstable angina, dyspnea or fatigue. The first symptoms of an AMI is usually the deep visceral pain, retrosternal, described as  oppressive, often radiating to the back, jaw or left arm. The pain has characteristics similar to those of angina pectoris, but usually is more intense, lasting and poorly or only transiently relieved by rest or nitroglycerin. However, pain can be very mild and about 20% of acute heart attacks are silent or not recognized by the patient as a pathological event. Women may have atypical chest discomfort. Elderly patients may complain of dyspnea rather than chest pain of ischemic type. In severe episodes, the patient appears anxious and may experience a feeling of impending doom. You may experience nausea and vomiting, particularly lower in the IM. The symptoms of LV failure, pulmonary edema, shock or significant arrhythmias may dominate the clinical picture.

On clinical examination, the patient is in the grip of an intense pain, are usually restless and anxious, with skin pale, cold and sweaty. Peripheral or central cyanosis may occur. The pulse may be wiry and BP is variable, although most patients initially present some degree of hypertension, unless you are developing cardiogenic shock.

The heart sounds are often a bit 'muffled, almost as a rule the presence of a quarter tone. There may be a mild apical systolic murmur (an expression of dysfunction of the papillary muscle). The importance of rubbing or blowing stronger initial assessment suggests a pre-existing heart disease or another diagnosis. The appearance of a rub in the first hours is unusual and may suggest the diagnosis of acute pericarditis rather than IMA. Pericardial friction, usually evanescent, and are common to two or three days after a heart attack.