Right ventricular infarction following percutaneous coronary rotational atherectomy

Hetterich, Frank S.; McEniery, Paul T.

doi:10.1002/ccd.1810340210

Cited by 3 publications

(1 citation statement)

References 8 publications

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“…16,17 Proximal lesion angioplasty may result in compromise of RV branches, resulting in RV ischemic dysfunction despite an otherwise patent RCA and previously normal RV. 22 Therefore, we cannot exclude the possibility that some patients in the present study may have suffered such selective branch compromise, which influenced RV function. Finally, although our observations support those of previous studies that emphasize the importance of the status of RV branch perfusion to RV performance, whether selective recanalization of persistently occluded or stenosed RV branches improves RV performance in patients with otherwise patent arteries will need to be clarified in future studies.…”

Section: Discussionmentioning

confidence: 86%

Patterns of Coronary Compromise Resulting in Acute Right Ventricular Ischemic Dysfunction

et al. 2002

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Background-Although proximal right coronary artery (RCA) occlusion is the culprit commonly responsible for acute right ventricular (RV) infarction (RVI), the severity of RV dysfunction ranges broadly. This study was designed to delineate the patterns of coronary compromise that determine the magnitude of RV ischemic dysfunction. Methods and Results-In 125 patients with acute inferior myocardial infarction undergoing emergency angiography, the culprit infarct lesion was identified, RV branch flow assessed (TIMI flows and frame counts), and individual patient RV perfusion indices calculated by separately averaging the branch flows and frame counts, which were correlated with RV wall motion by ultrasound. RVI occurred in 53 (42%) patients, with the RCA as the culprit vessel and the lesion sufficiently proximal to compromise flow in at least one RV branch in all cases, thereby resulting in depressed RV perfusion (flow index, 0.7Ϯ0.2). In patients without RVI, the RCA was the culprit in 89%; the circumflex, in 11%. RCA culprits were proximal in 19% of such cases, with lack of RVI explained by preserved RV perfusion (flow index, 2.7Ϯ0.3; Pϭ0.001) attributable to at least 1 patent RV branch, spontaneous reperfusion, or prominent collaterals.Overall, there was a strong correlation between RV perfusion and wall motion (Spearman correlation coefficientϭ0.79). Conclusions-Proximal RCA occlusion compromising RV branch perfusion commonly results in RV ischemic dysfunction. In some cases with proximal RCA culprits, collaterals or spontaneous reperfusion preserve RV performance.

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Section: Discussionmentioning

confidence: 86%

Patterns of Coronary Compromise Resulting in Acute Right Ventricular Ischemic Dysfunction

et al. 2002

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Risk Factors for the Development of Slow Flow During Rotational Coronary Atherectomy

Sharma

Dangas

Mehran

et al. 1997

The American Journal of Cardiology

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Pathophysiology and management of right heart ischemia

Goldstein

2002

Journal of the American College of Cardiology

221

137

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Acute right coronary artery occlusion proximal to the right ventricular (RV) branches results in right ventricular free wall dysfunction, exerting mechanically disadvantageous effects on biventricular performance. Depressed RV systolic function decreases transpulmonary delivery of left ventricular (LV) preload, resulting in diminished cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction and septally mediated alterations in LV compliance, which are exacerbated by elevated intrapericardial pressure. Under these conditions, RV pressure generation and output are dependent on LV-septal contractile contributions, governed by both primary septal contraction and paradoxical septal motion. When the culprit coronary lesion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling and performance, resulting in more severe hemodynamic compromise. Bradyarrhythmias limit output generated by the rate-dependent noncompliant ventricles. Hemodynamic compromise may respond to volume resuscitation and restoration of physiologic rhythm. Vasodilators and diuretics should generally be avoided. In some patients, parenteral inotropic stimulation may be required. The right ventricle appears to be relatively resistant to infarction and recovers even after prolonged occlusion. The term RV "infarction" appears to be somewhat of a misnomer, for in most patients acute RV dysfunction represents ischemic but predominantly viable myocardium. Although RV performance improves spontaneously even in the absence of reperfusion, recovery of function may be slow and associated with high in-hospital mortality. Reperfusion enhances recovery of RV performance and improves the clinical course and survival.

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Right ventricular infarction following percutaneous coronary rotational atherectomy

Cited by 3 publications

References 8 publications

Patterns of Coronary Compromise Resulting in Acute Right Ventricular Ischemic Dysfunction

Patterns of Coronary Compromise Resulting in Acute Right Ventricular Ischemic Dysfunction

Risk Factors for the Development of Slow Flow During Rotational Coronary Atherectomy

Pathophysiology and management of right heart ischemia

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