Right ventricular myocardial infarction

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Acute myocardial infarction involving only the free wall of the right ventricle is a rare event. ^[1] More commonly, right ventricular infarction is associated with infarction of the inferior wall of the left ventricle, occurring in more than one-third of such cases,^{[2] [3] [4] [5] [6] [7] [8] [9] [10]} even when a thrombolytic therapy is given. ^[11]

One study of 113 patients with a first acute inferior wall infarction reported that the presence of preinfarction angina within 72 hours of the infarction was associated with a reduction in the incidence of right ventricular infarction (odds ratio 0.2) and combined hypotension and shock (odds ratio 0.1). ^[12] This is possibly the result of ischemic preconditioning.

• Ninety percent of right ventricular infarcts result from occlusion of the proximal right coronary artery, while another 5 to 10 percent arise after occlusion of the left anterior descending artery ^{[13] [14] [15] [16]}

Although more than one-third of cases are clinically silent ^[17], the presence of right ventricular infarction often has important implications for both management and prognosis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

ST elevation myocardial infarction is largely influenced by the role of plaque rupture.

Atherosclerosis, or hardening of the arteries, is the gradual buildup of cholesterol and fibrous tissue (collagen and smooth muscle cells) throughout the vascular tree. When there is localized accumulation of lipids and scar tissue, this is called a “plaque”. Somewhat paradoxically, it is not the most severe plaque narrowing that leads to ST elevation MI. Pathological studies indicate that it is often mild-to-moderate, lipid-laden, inflamed plaques that are the ones most likely to rupture and cause an ST elevation MI (STEMI) or a non ST elevation MI (NSTEMI). ^[1] The role of plaque rupture in STEMI and NSTEMI is supported by studies demonstrating that plaque rupture is present in about 70% and superficial erosion is present in 30% of patients who die suddenly in whom there is documented coronary artery disease. ^[2] Exposure of the blood stream to the thrombogenic components of the plaque leads to activation of the coagulation cascade and thrombus formation. In STEMI, the clot completely occludes the epicardial artery, and there is a complete lack of blood flow to the involved territory. This causes transmural injury and ST elevation. In NSTEMI, there is partial obstruction with embolization. This causes ischemia and subendocardial injury that are manifested by ST depression.

1. Macrophage accumulation has been shown to be present to a greater degree in patients with acute coronary syndromes than in those patients with chronic stable angina ^{[3] [4]} These activated macrophages can release enzymes such as metalloproteinases, interstitial collagenase, gelatinase, and stromelysin that degrade collagen, elastin, and proteoglycans. ^[5] This enzymatic degradation in turn leads to breakdown of the fibrous cap. The thin shoulders or edges of the fibrous cap appear to be particularly vulnerable to erosion and breakdown.
2. Neovascularization of the plaque Moreno et have shown that microvessel density was increased in ruptured plaques when compared with nonruptured plaques (P=0.0001). Furthermore, among lesions with severe macrophage infiltration at the fibrous cap, microvessel density was increased (P=0.0001) was well as at the edges or shoulders of the plaque (P=0.0001). Intraplaque hemorrhage was also associated with an increase in microvessel density (P=0.04) as was the presence of thin-cap fibroatheromas (P=0.038). Microvessel density at the base of the plaque was identified as an independent (P=0.003) correlate of plaque rupture. ^[6]
3. High oscillatory shear stress
4. Vasoconstriction
5. Spontaneous coronary dissection

There are numerous systemic risk factors associated with thrombus formation following plaque rupture:

1. Smoking: Smoking increases platelet aggregation and plasma epinephrine levels ^[7]
2. Fibrinogen: Elevated levels of fibrinogen have been associated with thrombosis including abnormal levels of fibrinogen ^[8]
3. Von Willebrand factor antigen ^[8]
4. Tissue plasminogen activator ^[8]
5. Anticardiolipin antibodies ^[9]
6. Cross-linked fibrin-degradation products ^[10]
7. Polymorphisms of a platelet glycoprotein receptor ^[11]

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

In 1940, Blumgart ligated or tied off the coronary artery in dogs and cats and for the first time demonstrated a wavefront of cell death folllowing vessel occlusion ^{[12] [13] [14] [15] [16]}

Irreversible injury of ischemic myocytes occurs first in the subendocardial zone. With more extended ischemia, a wavefront of cell death moves through the myocardium to involve progressively more of the transmural thickness of the ischemic zone. The precise location, size, and specific morphologic features of an acute myocardial infarction depend on:

1. The location, severity, and rate of development of coronary atherosclerotic obstructions,
2. The size of the vascular bed perfused by the obstructed vessels
3. The duration of the coronary artery occlusion
4. The metabolic / oxygen needs of the myocardium at risk,
5. The extent of collateral blood vessels

Decrease of ATP levels in myocytes in reaction to ischemia starts within seconds and causes loss of contractility in first two minutes. If ischemia persists, ATP levels reduced to its half level within 10 minutes and to 1/10 within 40 minutes. Irreversible cell injury occurs between 20-40 minutes and microvascular level injury starts if ischemia lasts more than an hour.^[17]

If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction.^[18] As a result, the patient’s heart can be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias.

In ST segment myocaridal infarction (STEMI), the ST segments on the ECG are by definition elevated and there is myonecrosis (death of myocytes) as reflected by elevation of biomarkers such as creatine kinase MB fraction (CK-MB) or troponin T or I (tn). The ST segments are elevated due to full thickness injury of the myocardium.

The following are excellent videos demonstrating the underlying pathophysiology. {{#ev:youtube|L6EiPLli5x8}} {{#ev:youtube|cOMzh2hf_Vw}} {{#ev:youtube|a8Idk4EUYTs}}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

• Acute myocardial infarction involving only the free wall of the right ventricle is a rare event. ^[1] More commonly, right ventricular infarction is associated with infarction of the inferior wall of the left ventricle, occurring in more than one-third of such cases. ^{[2] [3] [4] [5] [6] [7] [8] [9] [10]}, even when thrombolytic therapy is given ^[11]

• Ninety percent of right ventricular infarcts result from occlusion of the proximal right coronary artery.
• Another 5 to 10 percent arise after occlusion of the left anterior descending artery. ^{[12] [13] [14] [15]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

• Acute pericarditis
• Constrictive pericarditis
• Cor Pulmonale
• Endomyocardial fibrosis
• Hypertrophic Cardiomyopathy
• Pneumothorax
• Primary pulmonary hypertension
• Pulmonary Embolism
• Restrictive cardiomyopathy
• Secondary pulmonary hypertension
• Tricuspid Regurgitation

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Yuri B. Pride, M.D. [2] ; Cafer Zorkun, M.D., Ph.D. [3]

Myocardial infarction is a common presentation of ischemic heart disease. The World Heart Organization (WHO) estimated in 2002 that, 12.6 percent of deaths worldwide were from ischemic heart disease.

Ischemic heart disease is the leading cause of death in developed countries, but third to AIDS and lower respiratory infections in developing countries.^[1]

Over 9 million patients in the United States alone have angina. An estimated 80,700,000 American adults (one in three) have one or more types of cardiovascular disease (CVD), of whom 38,200,000 are estimated to be age 60 or older. Except as noted, the estimates were extrapolated to the U.S. population in 2005 from NHANES 1999–2004. (Total CVD includes diseases in the bullet points below except for congenital heart disease). Due to overlap, it is not possible to add these conditions to arrive at a total. ^{[2] [3][4]}

• Hypertension: 73,000,000
• Coronary heart disease: 16,000,000

• Myocardial infarction: 8,100,000
• Angina pectoris: 9,100,000

• Heart failure: 5,300,000
• Stroke: 5,800,000
• Congenital heart disease: 650,000 – 1,300,000

This means that roughly every 65 seconds, an American dies of a coronary event.

Although it is difficult to ascertain the true incidence of ST elevation myocardial infarction (STEMI), according to the ACC/AHA guidelines, a conservative estimate is that approximately 500,000 patients suffer STEMI each year ^[5]. The incidence of STEMI has decreased over time. In an observational study of 5,832 metropolitan patients spanning from 1975 to 1997, the incidence of STEMI decreased from 171/100,000 to 101/100,000 ^[6]

The following prevalence estimates are for people age 18 and older from NCHS/NHIS, 2005: ^[7]

• Among whites only, 12.0% have heart disease, 6.6% have CHD, 21.0% have hypertension and 2.3% have had a stroke.
• Among blacks, 10.2% have heart disease, 6.2% have CHD, 31.2% have hypertension and 3.4% have had a stroke.
• Among Hispanics or Latinos, 8.3% have heart disease, 5.9% have CHD, 20.3% have hypertension and 2.2% have had a stroke.
• Among Asians, 6.7% have heart disease, 3.8% have CHD, 19.4% have hypertension and 2.0% have had a stroke.
• Among Native Hawaiians or other Pacific Islanders, 22.4% have hypertension (other prevalence estimates considered unreliable).

The mortality among patients who suffer STEMI has progressively declined in recent years. From 1975 to 1997, one observational study reported that the in-hospital mortality decreased from 24% to 14% ^[6]. In the Global Registry of Acute Coronary Events (GRACE), a multinational cohort study that includes 16,814 patients with STEMI were enrolled and followed up in 113 hospitals in 14 countries between 1999 and 2006, in-hospital mortality declined from 8.4% in 1999 to 4.6% in 2005 ^[8].

The reason for this decline in mortality is likely multifactorial and includes, but is certainly not limited to, decline in symptom onset-to-presentation time, more widespread use of primary PCI ^[9], improvements in time to reperfusion (door-to-needle and door-to-balloon times) ^[10][11] and improved medical therapy, including increases in the use of evidence-based therapies such as aspirin ^[12], beta blockers^{[13] [14]}, clopidogrel ^[15], statins ^[16] and angiotension converting enzyme inhibitors or angiotensin receptor blockers ^[17].

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

In these chapters on ST elevation, the word risk factors refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing atherosclerotic plaque. The word triggers refer to those factors in the patients immediate history or environment that may have lead to rupture of the atherosclerotic plaque.

Muller et al have developed the following nomenclature to categorize and analyze data pertaining to triggers of MI ^[1]:

(1) Trigger: An activity that produces short-term physiological changes that may lead directly to onset of acute CVD.

(2) Acute risk factor: A short-term physiological change, such as a surge in arterial pressure or heart rate, an increase in coagulability, or vasoconstriction, that follows a trigger and may result in disease onset.

(3) Hazard period: The time interval after trigger initiation associated with an increased risk of disease onset because of the trigger. The onset and offset times of the hazard period, which could also be designated a “vulnerable period,” may be sharply defined, as in heavy exertion, or less well defined, as with respiratory infection. The duration of the hazard period may also vary, eg from < 1 hour during heavy physical exertion to weeks or months with bereavement.

(4) Triggered acute risk prevention (TARP): Cardiovascular risk reduction that focuses on the short-term increase in risk associated with a trigger.

Risk factors for atherosclerosis are generally risk factors for myocardial infarction:

• Advancing age
• Male gender^[3]
• Cigarette smoking
• Hypercholesterolemia (more accurately hyperlipoproteinemia, especially high low density lipoprotein and low high density lipoprotein)
• Diabetes (with or without insulin resistance)
• High blood pressure
• Obesity^[4] (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).
• Elevated homocysteine

• Mendelian inherited conditions

Familial mixed hyperlipidaemia

LDL receptor deficiency

• Autosomal dominant conditions

Pseudoxanthoma elasticum dominant type 1

• Autosomal recessive conditions

Cystathionine beta-synthase deficiency

Sitosterolemia

According to present trends in the United States, half of healthy 40-year-old males and 1 in 3 healthy 40-year-old women will develop coronary artery disease (CAD) in the future.^[5] This chance is greater when a family history of heart disease is involved.

Studies have reported that the risk of CAD increases two- to sevenfold when there is a genetic link. ^[6] The studies by Nora and Nora (1978a) evaluated a large number of patients with congenital heart disease.^[7] Results show that about 8% of the defects were primarily genetics-related, 2% were environmental (caused by drugs, viruses, maternal nutrition, maternal metabolism, or fetal hemodynamics) and 90% were multifactorial (due to a combination of environmental and genetic factors). The study also noted that there is a two- to threefold increase in the recurrence risk for congenital heart disease when two of the family members are affected. This is particularly the case when the parent is severely affected or when the affected members are child and parent. The risk for a myocardial infarction is two to three times greater in a first-degree relative than in a person with no family history of heart disease. This fact speaks in particular to the early presentation of CAD in patients with no other risk factors. Second cousins have a 1 in 23 chance of sharing a particular gene and third cousins have a 1 in 128 likelihood.

Genetic hypertension and hyperlipidemia are strong predictors of familial heart disease.^[8] Hypertensive people are twice as likely to have a family history of the condition than are normotensives. Genetic hypertension is an example of a polygenic mode of inheritance that reflects cellular sodium transport defects and an abnormal response to psychogenic stress. There is indication that Pheochromocytoma, a rare cause of hypertension, may be familial as well.

• Diabetes mellitus type 2 (NIDDM)
• Primary hyperparathyroidism

• Systemic lupus erythematosus (SLE)

Socioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of MI.^[9] To understand epidemiological study results, it’s important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status.^[9]

Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.^[10]

Inflammation is known to be an important step in the process of atherosclerotic plaque formation.^[11] C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation. Elevated CRP blood levels, especially measured with high sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes.^[11] Moreover, some drugs for MI might also reduce CRP levels.^[11] The use of high sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician’s discretion, in patients who already present with other risk factors or known coronary artery disease.^[12] Whether CRP plays a direct role in atherosclerosis remains uncertain.^[11]

Inflammation in periodontal disease may be linked coronary heart disease, and since periodontitis is very common, this could have great consequences for public health.^[13] Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease.^[14] Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines;^[15] thus, periodontitis may mediate its effect on MI risk via other risk factors.^[16] Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells.^[17][18] A role for specific periodontal bacteria has been suggested but remains to be established.^[19]

Baldness, hair greying, a diagonal earlobe crease^[20] and possibly other skin features are independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.^[21]

While family history, along with age and sex, is uncontrollable^[3], many of the risk factors for heart disease can be eliminated by maintaining a healthy lifestyle. In fact, a person’s daily habits significantly affect the risk of heart disease due to genetic predisposition. Studies have shown that deaths can be avoided by attending to the controllable risk factors. Such risk factors include: obesity, blood pressure, cigarette smoking and plasma cholesterol.^[22]

A study published in Circulation shines some light on the importance of eliminating these controllable risk factors in people with a family history of heart disease. Data demonstrated that in men with a genetic link to heart disease, an estimated 68% of the excess deaths were due to the addition of smoking, a modifiable risk factor; concluding that the risk of heart disease in men with a family history of the condition is significantly related to the additional risk factors he accumulates.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The presence of right ventricular infarction adversely affects the early prognosis. Elderly patients who have right ventricular involvement with an inferior wall myocardial infarction are at particularly high risk. For patients who survive an acute right ventricular infarction, however, the prognosis is generally good.

• The presence of right ventricular infarction adversely affects the early prognosis. One study, for example, evaluated 200 consecutive patients with acute inferior myocardial infarction. ^[1] Those with ST elevation in V4R had an almost eight-fold increase in in-hospital mortality (31 versus 6 percent) and morbidity when compared to those without changes in V4R.
• Elderly patients who have right ventricular involvement with an inferior wall myocardial infarction are at particularly high risk. In a study of 198 patients ≥ 75 years of age, right ventricular involvement was associated with an in-hospital mortality of 47 percent compared to a 10 percent mortality in the absence of right ventricular involvement ^[2]
• For patients who survive an acute right ventricular infarction, however, the prognosis is generally good. As an example, among 522 patients with an inferior wall infarction who were treated with a thrombolytic agent and hirudin or heparin in the HIT-4 study, 32 percent had right ventricular involvement and these patients had a higher 30 day mortality when compared to those without right ventricular involvement (5.9 versus 2.5 percent. ^[3] However, this was related to a larger infarct size rather than right ventricular involvement; right ventricular involvement was not an independent predictor of survival.
• The right ventricle frequently recovers the majority of its function, probably due at least in part to a decreased oxygen demand of the thin-walled right ventricle. ^{[4] [5]} These patients may, however, have a more frequent requirement for a permanent pacemaker. ^[6]

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