Ischemic heart disease (IHD) is the leading cause of death around the world. IHD develops, when coronary arteries become narrowed and it is mainly due to atherosclerosis. Many people don't know they have IHD, until they develop angina or a heart attack.
Aim: To know the etiology, risk factors, symptoms, morphology of myocardial infarction and complications.
Etiology: IHD is due to accumulation of lipoproteins, which lead to formation of the atheromatous plaque that will narrow the coronary artries and decrease the blood supply to the heart leading to ischemia. The resulting ischemia may be complicated by myocardial infarction.
Risk factors: They are divided into controllable (High blood pressure, high cholesterol, smoking, diabetes, stress, Being overweight or obese) and non-controllable risk factors (as family history, age and gender).
Morphology of myocardial infarction: The myocardium shows coagulative necrosis and centeral yellow area surrounded by hyperemic border. The scar completes after 2 months. Microscopically, there is hypereasinophilic myocyte with loss of the nuclei with phagocyte infiltration, which appears basophilic. The coronary artery shows thrombosis and the plaque may ulcerate.
Complications: They may include: acute pulmonary edema, heart rupture (left ventricular wall rupture, ventricular septal rupture and papillary muscle rupture), left ventricular aneurysm, ventricular pseudoaneurysm, carcinogenic shock, pericarditis and pulmonary hemorrhage, arrhythmia and sudden death from lethal arrhythmia.
Introduction:-
The IHD is has one of the highest mortality rates around the world. It develops mainly, when arteries of the heart become too narrow. Many risk factors can increase the chance of developing IHD. It has very serious complications discussed in this review.
Aim: To know the etiology, risk factors, clinical symptoms, morphology of myocardial infarction and complications.
Etiology:-
IHD is a cardiovascular disorder occurring due to atherosclerosis or atherosclerotic occlusions of the coronary arteries in most cases (Mendis et al., 2011).
When the endothelial function of the arterial wall disrupts, atherosclerosis begins due to the accumulation of lipoprotein droplets in the intima of the coronary vessels (Badimon et al., 2012).
Plaque can start to collect along the blood vessel walls, when we are young, building up gradually as we get older. That buildup inflames the vessel walls and raises the risk of blood clot and heart attack. The plaque makes the inner walls of the blood vessels sticky. Some Things like inflammatory cells, lipoproteins, and calcium attach to this plaque while travelling through the bloodstream.
As a result of accumulation of more of these materials along with cholesterol, the artery walls become narrower & obstruction of blood flow may occur, which leads to a mismatch between myocardial oxygen demand and supply (Cassar et al., 2009).
Risk Factors:-
There is no single cause for coronary heart disease, but 'the risk factors' can increase your chance of developing it.
A. Controllable risk factors: (controlled through lifestyle changes and medication)
Smoking: It promotes coronary occlusion, as it produces endothelial denudation and platelet adhesion to subintimal layers, thereby increasing the build of fatty materials and platelet‐derived growth factor‐mediated proliferation of smooth muscle cells, which narrows the artery. Smokers have been reported to have 70% more IHD mortality than non-smokers (US Department of Health and Human Services, 1990).
Diabetes: particularly, diabetes mellitus or type 2 diabetes (Haffner, 1999).
Cholesterol: Low levels of high-density lipoprotein cholesterol, high levels of very low‐density lipoprotein (VLDL) cholesterol & high levels of total VLDL triglycerides have been reported as risk factors for IHD in patients with type2 diabetes (Laakso et al., 1993).
Blood Pressure: Atherosclerosis could be aggravated by arterial hypertension. Hypertension has also been frequently associated with metabolic disorders like insulin resistance or hyperinsulinemia and dyslipidemia, which are known to be risk factors of IHD (DeFronzo & Ferrannini, 1991).
Obesity: Excess body fat in the abdominal visceral could lead to atherosclerotic disease (Matsuzawa et al., 1995).
Hyperuricemia: Some studies have indicated an association between hyperuricemia and the risk of IHD (Zalawadiya et al., 2015).
Stress: Various physiological changes produced by stress (such as elevated blood pressure, reduced insulin sensitivity, elevated hemostasis, and endothelial dysfunction) may be relevant to cardiovascular diseases (Steptoe & Kivimäki, 2012).
B. Uncontrollable risk factors:-
Family history: It is an important determinant of IHD risk, but one that is hard to quantify (Pandey et al., 2013).
Age: The risk of IHD increases with age (Teramoto et al., 2013).
Gender: Men are more liable to develop IHD at an earlier age than women. However the risks increase in postmenopausal women (Stangl et al., 2002).
Ethnicity: Asian indians have a higher risk of heart disease as compared to other ethnic origins (Enas et al., 2001).
Clinical presentation:-
Angina pectoris: It is a chest pain on exertion, in cold weather or in emotional situations. Patients may experience nausea, vomiting, sweating and enhanced anxiety (Kosuge et al., 2006).
Myocardial infarction, heart failure & sudden cardiac death (Kannel, 2002).
Morphology of myocardial infarction in pre & post interventional era: The pathological diagnosis of myocardial infarction depends on the coagulative necrosis of the myocardium, repairing feature and detection of thrombosis in the coronary arteries (Robbins & Cortan, 2005).
Myocardium: The non reperfused myocardial infarction shows coagulative necrosis (Robbins & Cortan, 2005). 12-14 hours the myocardium is dark motling. 1-3 days there is centeral yellow area surrounded by hyperemic border. 7-10 days the border gets red-gray. 7-8 weeks the scar starts from the periphery to the center. After 2 months the scar completes. The microscopic appearance before 12 hours, there is hypereasinophilic change in the myocyte, but it's poorly informative (Madrigal et al., 1979). After 12 hours start of coagulative necrosis with loss of the nuclei. The neutrophilic infiltration begins from 1-3 days (figure 3). Day 3-7 phagocytosis of the border and fragmentation of the myocyte. After 1 week beginning of the granulation tissue. Dense collagen deposits (3-8 weeks). Complete scar develops in the second month (Robbins & Cortan, 2005). After 2 months the collagen becomes dense and compact and the myocardium is acellular.
Coronary artery:-
A plaque with thrombosis is found at autopsy in about 90% of patients died from myocardial infarction and not treated by thrombolysis or percutaneous coronary angioplasty. The plaque ruptured in about 75% of cases and erosion in minority of cases (Arbustini et al., 1999). The lesion is large atherosclerotic plaque with cap ulceration and superimposed thrombosis. The thrombosis is red with small platelets (in the head), fibrin and red cells (in the body & tail) (Arbustini et al., 1991).
Post thrombolytic & post percutaneous coronary angioplasty era:
Reperfusion in myocardial infarction restores the coronary flow using thrombolytic and percutaneous coronary angioplasty (Antman et al., 2004). The great effectiveness occurs with percutaneous coronary angioplasty, when done within the first 12 hours from the beginning of the ischemia (Abustini et al., 1999).
Morphology of myocardium:-
The gross appearance of the reperfused myocardial infarction is hemorrhagic. The microscopic examination shows coagulative necrosis with red cells infarction (figure 4).
The small vessels show thromboembolism. The vessels may be damaged and worsen the hemorrhagic invasion. This may lead to swelling of the cells and may prevent the reperfusion (non-reflow) phenomenon (Rezkalla & kloner, 2002). If the reperfusion occurs before the necrosis, the area at the risk will be rescued. The scar of the reperfused myocardial infarction has more angiogenesis than non-reperfused one. The result of the reperfusion is limitation of the infarction and improvement of the function (Antman, 2004).
The reperfused myocardial infarction culprit is expected to be patent. It may show hemorrhagic invasion, thrombosis and ulceration (Prati et al., 2003). New filters are used to collect thrombosis and plaque to limit the small vessels impairment (Stone et al., 2005).
Myocardial infarction complications:-
• Acute pulmonary edema:
Pulmonary edema is associated with a 20-40% 30-day mortality rate, It occurs as an acute event with the beginning of ST-elevation myocardial infarction (STEMI) or reinfarction or as the climax of slowly progressive congestive heart failure during the first days after myocardial infarction (MI) (Pena-Gil et al., 2005).
• Heart rupture:
a) Left ventricular free-wall rupture occurs in 1-6% of all patients admitted with STEMI. Risk factors include: first MI, anterior infarction, old age, female sex, hypertension, no collater,als, and intake of corticosteroids or non-steroidal anti-inflammatory drugs. The main determinants in preventing rupture are early reperfusion and collateral circulation (Nakumura et al., 1992) (Pallak et al., 1994).
b) Ventricular septal rupture rarely occurs. The frequency of acute rupture of inter-ventricular septum declines during reperfusion period. Rupture site can rapidly expand and cause sudden hemodynamic collapse (Crenshaw et al., 2000).
c) Papillary muscle rupture rarely occurs. The diagnosis is made on the basis of clinical and imaging findings.
Left ventricular aneurysm:
It occurs in the left anterior wall, combined with left anterior descending occlusion and wide infarcted area (Tikiz et al, 2001).
Ventricular pseudoaneurysm:
It is a rare complication. It occurs as a result of rupture of ventricular free wall and is covered by overlying adherent pericardium. The pathologic features depend on interval of time between beginning of MI & death and also the extent of hemorrhage. The myocardial wall shows fissuring. Coagulative necrosis is one of the myocardial changes (Neven et al, 2005).
Arrhythmias:
They are common in patients with STEMI and occur early after development of symptoms. The mechanisms for ventricular tachyarrhythmia include loss of transmembrane resting patients, development of foci of enhanced automaticity (Carmeliet, 1999).
Lethal arrhythmias / sudden death:
They are one of the most common causes of death in non-hospitalized patients with acute MI (Perron & Sweeney, 2005).
Cardiogenic shock:
It is frequently caused by extensive left ventricular dysfunction, other common causes include mechanical complications (acute mitral regurgitation & ventricular septal rupture) (Hochman, 2003).
Mitral regurgitation (MR):
It occurs as a consequence of papillary muscle, lateral wall infarction. It has poor diagnosis if accompanied with cardiogenic shock. The area of infarction seems to be less extensive in case of papillary muscle and wall infarction than papillary displacement (Hochman, 2003).
Pericarditis:
It occurs in transmural STEMI including the whole thickness of the myocardial wall to the epicardium. Patients with pericarditis have larger infarcts, lower ejection fraction and higher risk of congestive heart failure (Shahar et al., 1994).
Acute pulmonary hemorrhage:
It is a rare complication that occurs in patients who undergo primary percutaneous transluminal coronary angioplasty (PTCA) and are treated with glycoprotein IIb/IIIa inhibitors. The pathological diagnosis is important to confirm the alveolar invasion by red blood cells. Bleeding complications are common in women than in men (Razakjr et al., 2005) (Ali et al., 2003).
Conclusion:
IHD is the leading cause of death worldwide and have many risk factors (as high cholesterol, smoking, diabetes, obesity, hypertension & aging). It has very serious complications (as pulmonary edema, aneurysm, rupture arrhythmia & carcinogenic shock).