Right ventricular infarction was first recognized in a subgroup of patients with inferior wall myocardial infarctions who demonstrated right ventricular failure and elevated right ventricular filling pressures despite relatively normal left ventricular filling pressures. Increasing recognition of right ventricular infarction, either in association with left ventricular infarction or as an isolated event, emphasizes the clinical significance of the right ventricle to total cardiac function.
Interest in recognizing right ventricular infarction noninvasively has grown because of the therapeutic implications of distinguishing patients with right ventricular dysfunction from those with the more usual clinical presentation of left ventricular dysfunction. Patients with right ventricular infarctions associated with inferior infarctions have much higher rates of significant hypotension, bradycardia requiring pacing support, and in-hospital mortality than isolated inferior infarctions.[1]
For more information, see Myocardial Infarction.
NextPathophysiologyThe right ventricle is a thin-walled chamber that functions at low oxygen demands and pressure. It is perfused throughout the cardiac cycle in both systole and diastole, and its ability to extract oxygen is increased during hemodynamic stress. All of these factors make the right ventricle less susceptible to infarction than the left ventricle.
The posterior descending branch of the right coronary artery usually supplies the inferior and posterior walls of the right ventricle. The marginal branches of the right coronary artery supply the lateral wall of the right ventricle. The anterior wall of the right ventricle has a dual blood supply: the conus branch of the right coronary artery and the moderator branch artery, which courses from the left anterior descending artery.[2]
Interestingly, right ventricular infarction noted at necropsy usually involves the posterior septum and posterior wall rather than the right free wall. The relative sparing of the right ventricular anterior wall apparently arises from a high degree of collateralization. This collateral blood flow is thought to be derived from the thebesian veins and diffusion of oxygen directly from the ventricular cavity. A direct correlation exists between the anatomic site of right coronary artery occlusion and the extent of right ventricular infarction. Studies have demonstrated that more proximal right coronary artery occlusions result in larger right ventricular infarctions.[3] On occasion, the right ventricle can be subjected to infarction from occlusion of the left circumflex coronary artery.[4]
Because the right ventricle is considered a low-pressure volume pump, its contractility is highly dependent on diastolic pressure. Hence, when contractility and associated diastolic dysfunction are impaired attendant to right ventricular infarction, the right ventricular diastolic pressure increases substantially and systolic pressure decreases. In such a scenario, concomitant left ventricular dysfunction, with increase in right ventricular afterload, is possible. In such a setting, right ventricular output can decrease dramatically, and the only driving force remaining is elevated right atrial pressure. In such a circumstance, the right ventricle serves as a poorly functioning conduit between the right atrium and the pulmonary artery.
Elevation of right atrial pressure secondary to right ventricular infarction has been noted to serve as a stimulus for secretion of atrial natriuretic factor. Increased levels of this polypeptide can be detrimental to normal left ventricular filling pressures. This occurs by virtue of the potent vasodilating, natriuretic, diuretic, and aldosterone-inhibiting properties of atrial natriuretic factor. Inappropriately elevated levels of atrial natriuretic factor may worsen the clinical syndrome of right ventricular infarction.[5] The potential hemodynamic derangements associated with right ventricular infarction render the afflicted patient unusually sensitive to diminished preload (ie, volume) and loss of atrioventricular synchrony. These 2 circumstances can result in a severe decrease in right and, secondarily, left, ventricular output.[6, 7, 8]
Early thrombolysis or mechanical reperfusion of an occluded coronary artery resulting in right ventricular infarction is associated with prompt reduction in right atrial pressure. This is extremely important because persistently elevated right atrial pressure has been associated with increased in-hospital mortality when associated with myocardial infarction. The extent of right ventricular infarction varies greatly and is dependent on the site of occlusion of the right ventricular arterial supply. If occlusion occurs before the right ventricular marginal branches and if collateral blood flow from the left anterior descending coronary artery is absent, then the size of infarction generally is greater. Extent of infarction depends somewhat on flow through the thebesian veins.[9, 10] In general, any major reduction in blood supply to the right ventricular free wall portends an adverse prognosis in association with this disorder.
PreviousNextEpidemiologyIsolated infarction of the right ventricle is extremely rare; right ventricular infarction usually is noted in association with inferior wall myocardial infarction. The incidence of right ventricular infarction in such cases ranges from 10-50%, depending on the series.[11]
The frequency of right ventricular infarction, which can be detected by right-sided precordial leads, in association with non–ST-segment elevation or non–Q-wave myocardial infarction, is not known and currently is being investigated. Although right ventricular infarction is clinically evident in a sizable number of cases, the incidence is considerably less than that found at autopsy.[12, 13, 10, 14] A major reason for the discrepancy is the difficulty in establishing the presence of right ventricular infarction in living subjects. Additionally, right ventricular dysfunction and stunning frequently are of a transient nature, such that estimation of its true incidence is even more difficult.
Criteria have been set forth to diagnose right ventricular infarction; even when strictly employed, however, the criteria lead to underestimation of the true incidence of right ventricular infarction.[15, 16, 17]
PreviousProceed to Clinical Presentation , Right Ventricular Infarction
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