Ischemic heart diseases Dr. Gehan mohamed Dr. Abdelaty shawky

Ischemic Heart Disease (IHD) * Causes: Usually caused by decreased coronary artery blood flow (“coronary artery disease”) as in: 1. Coronary artery atherosclerosis. 2. Vasospasm and vasculitis.

Ischemic Heart Disease (Coronary Heart Disease) * There are Four syndromes: 1. Angina pectoris (chest pain). 2. Myocardial infarction. 3. Chronic ischemic heart disease with congestive heart failure. 4. Sudden cardiac death. in the vast majority of cases, IHD is due to a reduction in coronary blood flow caused by obstructive atherosclerotic disease Thus, IHD is also frequently called coronary artery disease (CAD).

* Epidemiology of Ischemic Heart Disease: Peak incidence: 60y for males and 70y for females. Gender: Men are more affected than women. Risk factors: are that of atherosclerosis: Hypertension. Diabetes mellitus. Smoking. High levels of LDL. Genetic factors (direct or indirect). Lack of exercise.

* Pathogenesis Ischemic Heart Disease(IHD) : Four different factors play a role in the pathogenesis of IHD which include : 1. Role of critical stenosis or obstruction: (>75% of the lumen of one or more coronary arteries by atherosclerotic plaque).

Natural history of atherosclerosis

2. Role of acute Plaque Changes: a. Rupture of the plaque. b. Ulceration of the plaque. These expose the thrombogenic subendothelial basement membrane to blood followed by thrombosis . c. Hemorrhage into the plaque expanding its volume and aggravating the stenosis.

3. Role of coronary thrombosis: Thrombosis on partially stenotic plaque converts it to a total occlusion. this can lead to acute transmural myocardial infarction. When the extent of luminal obstruction by thrombosis is incomplete it usually leads to unstable angina, acute subendocardial infarction.

4. Role of vasoconstriction: Vasoconstriction reduces lumen size and can therefore potentiate plaque disruption.

Ischemic Heart Disease: Pathogenesis *the augmented coronary flow because of vasodilatation is insufficient to meet the increase in myocardial demand of O2.

A. Plaque rupture without superimposed thrombus in a patient who died suddenly. B. Acute coronary thrombosis superimposed on an atherosclerotic plaque with focal disruption of the fibrous cap, triggering fatal myocardial infarction. C. Massive plaque rupture with superimposed thrombus, also triggering a fatal myocardial infarction (special stain highlighting fibrin in red). In both

Angina pectoris

* Definition: paroxysmal and usually recurrent attacks of substernal chest discomfort (variously described as constricting, crushing, squeezing, choking, or knifelike). May radiate down the left arm or to the left jaw (referred pain) . * Cause: Transient inadequate myocardial perfusion (lasting for 15 seconds to 15 minutes)i.e. duration and severity is not sufficient for infarction.

There are three overlapping patterns of angina pectoris: 1. Stable or typical angina. 2. Unstable or crescendo angina. 3. Prinzmetal or variant angina.

1. Stable/ typical angina pectoris * Definition: Episodic chest pain associated with exertion or some other forms of stress. Usually relieved by rest or sublingual nitroglycerin (a strong vasodilator). The most common form of angina, caused by atherosclerotic disease.

2. Unstable or crescendo angina Definition: Pain occurs with progressively increasing frequency, is precipitated by less exertion, even at rest, and tends to be of more prolonged duration. Cause: disruption or rupture of an atherosclerotic plaque with superimposed partial thrombosis. Unstable angina is often the precursor of subsequent acute MI. Thus this referred to as pre-infarction angina.

3. Prinzmetal variant angina * Definition: uncommon pattern that occurs at rest and is due to coronary artery spasm and not related to atherosclerotic disease.

Myocardial Infarction

* Definition: coagulative necrosis of the myocardium due to acute coronary ischaemia. * Causes: The most common cause is thrombosis on a preexisting disrupted atherosclerotic plaque e.g. hemorrhage, ulceration and rupture…

* Sites of MI: I. Left ventricle (the commonest): a. Anterior infarct (anterior wall of the Lt .ventricle + apex + anterior part of IV septum): due to occlusion of the anterior descending branch of the left coronary artery. b. Lateral infarct (lateral wall of the Lt. ventricle): due to occlusion of circumflex branch of the left coronary. c. Posterior infarct (posterior wall of the Lt. ventricle): due to occlusion of a branch of the Rt. coronary artery that supplies that part of the left ventricle. II. Right ventricle (rare): due to occlusion of the right coronary artery.

Pathogenesis of MI

* Types of MI: Transmural Subendocardial Full thickness. Inner 1/3 of myocardium Transmural , sever coronary atherosclerosis with acute plaque rupture and superimposed thrombosis

* Morphologic changes of Myocardial Infarction: Time Gross changes Microscopic changes 0-4h None 4-12h Pale and firm Coagulation necrosis 12-24h Pale and soft More coagulation necrosis; neutrophils come in 1-7 d Yellow infarct center Neutrophils die, macrophages come to eat dead cells 1-2 w Yellow center, red borders Granulation tissue 2-8 w Scar Collagen

Acute Myocardial Infarction

MI: day 1, day 3, day 7

* Clinical Features of MI: 1. Pain: Severe crushing substernal chest pain, which may radiate to the neck, jaw, epigastrum, shoulder or left arm. Pain lasts for hours to days and is not relieved by nitroglycerin. Absent in 20-30% of patients (diabetics, hypertensive, elderly). 2. Pulse is rapid and weak. 3. Dyspnea. 4. Cardiogenic shock in massive MI(>40%of lt. ventricle). 5. ECG shows typical findings of ischemia.

* Laboratory evaluation of MI: 1. Troponins: The most specific test for MI. Become detectable within 2 to 4 hours, reach the peak at 48 hours. Their levels remain elevated for 7 to 10 days. 2. Creatine kinase (CK-MB): Is the second best marker, however, it increases in the blood also when there skeletal muscle damage. It begins to rise within 2 to 4 hours of MI, peaks at 48 hours and returns to normal within approximately 72 hours. 3. Lactate dehydrogenase (LD1). Rise 24 hrs, peaks 72 hrs, persists 72 hrs. Non-specific because it aslo increases in cases of cancer, encephalitis, meningitis… , total CK activity is not a reliable marker of cardiac injury (i.e., it could come from skeletal muscle injury). Although cardiac troponin and CK-MB are equally sensitive at early stages of an MI, persistence of elevated troponin levels for approximately 10 days allows the diagnosis of an acute MI long after CK-MB levels have returned to normal.

* Complications of MI: Cardiac arrhythmia: Occurs in more than 90% of cases. Cardiac arrhythmia: - Sudden death can occur due to ventricular arrhythmia. 2. Left ventricular failure. 3. Cardiogenic shock. 4. Myocardial rupture and hemopericardium. 5. Thromboembolism: The combination of a local myocardial abnormality in contractility (causing stasis) with endocardial damage (causing a thrombogenic surface) can foster mural thrombosis and, potentially, thromboembolism .

6. Pericarditis 7. Ventricular aneurysm. 8. Chronic heart failure.

Robbins and Cotran’s: Pathologic Basis of Disease. Seventh edition. Thanks References: Robbins and Cotran’s: Pathologic Basis of Disease. Seventh edition.