Ischemic right ventricular dysfunction

Abstract

For many years ischemic heart disease involving the right ventricle had received little attention. During the last 15 years, the initial works of Cohn, Isner, and others spawned a number of clinical and experimental studies that extended the understanding of the pathophysiology of ischemia in the right ventricle. Most of the work has been done in the setting of acute myocardial infarction, and information is still lacking in other conditions, such as chronic ischemic heart disease and perioperative right ventricular dysfunction. Acute right ventricular infarction rarely occurs in the absence of left ventricular necrosis and in most cases is the extension of an inferior left ventricular infarct. The majority of patients with right ventricular infarction only exhibit subtle signs of ischemic dysfunction. Elevated right atrial pressure is found only in the typical syndrome of elevated venous pressure; low output syndrome can be found only in 20% of the cases, and cardiogenic shock secondary to right ventricular necrosis is found only in 10%. It is also important to note that there is not a clear correlation between the severity of ischemic right ventricular dysfunction and the necrotic area. The discrepancy may be due to ischemia without necrosis of the right ventricular wall (stunned myocardium), but the intact pericardium and the necrosis of the interventricular septum may also play an important role. In the most severe form of ischemic right ventricular dysfunction, the entire right ventricular wall is akinetic. Right atrial, right ventricular, and pulmonary artery pressures become similar in magnitude and shape, and the pulmonary valve is opened during diastole, demonstrating a passive blood flow from the right atrium to the left ventricle through the low resistance pulmonary capillary bed. Volume loading, administration of dopamine or dobutamine, and careful use of vasodilators under hemodynamic monitoring are the therapeutic measures to control the severe forms of acute ischemic right ventricular dysfunction. The use of thrombolytic agents has decreased the incidence of right ventricular dysfunction after acute myocardial infarction. Mortality is high in the severe forms of acute ischemic right ventricular dysfunction, but after discharge from hospital the prognosis is good and right heart failure is unusual, even in those patients with shock during the first days of evolution of the infarct.

Cardioprotection in chronically hypoxic rabbits persists on exposure to normoxia: role of NOS and KATP channels

“…Clinically, cyanotic children undergoing repairs of heart defects manifest symptoms of right heart failure (8,15). There are little animal data analyzing the response of the right ventricle in response to ischemia and reperfusion.…”

Right ventricular enlargement predicts responsiveness to tolvaptan in congestive heart failure patients with reduced ejection fraction

“…Since tolvaptan can have a more favorable effect on patients with venous congestion [ 11 , 26 , 27 ], venous congestion may play a key role in responsiveness to tolvaptan. First, RV dilatation itself may be a reliable maker of venous congestion because RV dilatation was proven to represents right-sided volume overload and elevated filling pressure [ 28 , 29 ]. Second, patients with RV dilatation may tend to show RV diastolic dysfunction similar to that seen in constrictive pericarditis, and may have more severe venous congestion [ 24 , [30] , [31] , [32] , [33] , [34] , [35] ].…”

Epi and endomyocardial pH allows the detection of acute right ventricular ischemia in pigs: a new evaluation method

“…1 Right ventricular (RV) ischemia is particularly challenging to identify, as reliable identifying measures are difficult to obtain. Standard electrocardiographic (ECG) tracings are not specific; right-sided ECG monitoring, although more reliable in detecting RV ischemia, is not used commonly.…”