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Pathophysiology and management of right heart ischemia

^* Division of Cardiology, William Beaumont Hospital, Royal Oak, Michigan, USA

View larger version (149K): [in a new window]   Figure 1 Angiograms showing successful and unsuccessful reperfusion in patients with right ventricular infarction who underwent primary angioplasty. A shows total occlusion of the right coronary artery proximal to the right ventricular branches (arrow) in a patient before angioplasty, and B shows complete reperfusion after angioplasty, with a thrombolysis in myocardial infarction grade 3 flow in the right main coronary artery and its major right ventricular branches (arrowheads). C shows the complete failure of reperfusion in another patient, with impaired flow in the right main coronary artery, left ventricular branches, and right ventricular branches (arrowhead), attributable to refractory dissection and thrombus (arrows). D shows partial reperfusion in a third patient, with an absence of flow in the right ventricular branches, despite successful reperfusion of the right main coronary artery and its left ventricular branches. Reprinted with permission from reference 12.

View larger version (82K): [in a new window]   Figure 2 Echocardiographic images from a patient with acute inferior myocardial infarction and right ventricular ischemia in whom angioplasty was successful. Images at end-diastole (ED) and end-systole (ES) were obtained from the transthoracic apical four-chamber view. At baseline, there was severe right ventricular dilation with reduced left ventricular diastolic size at ED. At ES, there was right ventricular free-wall dyskinesis (arrows), intact left ventricular function, and compensatory paradoxical septal motion. One hour after angioplasty, there was a striking recovery of right ventricular free-wall contraction (arrows), resulting in marked improvement in global right ventricular performance, with a markedly reduced right ventricular size and an increased left ventricular size at end diastole. At one day, there was further improvement in right ventricular function (arrows), and at one month right ventricular size and function (arrows) were normal. RV = right ventricle; LV = left ventricle. Reprinted with permission from reference 12.

View larger version (33K): [in a new window]   Figure 3 Hemodynamic recordings from a patient with a W pattern. Peaks of W are formed by prominent A-waves, and most prominent right atrial (RA) descent occurs just before T-wave of electrocardiogram (ECG) (A). Simultaneous RA and right ventricular (RV) pressures (B) demonstrate that this prominent descent coincides with peak right ventricular systolic pressure (RVSP) and is therefore an "X" systolic descent, followed by a comparatively blunted Y descent. Peak RVSP is depressed, RV relaxation is prolonged, and there is a dip and rapid rise in RV diastolic pressure. Prominent RA A-waves are reflected in the right ventricle as an augmented end-diastolic pressure (EDP) rise (arrows). These waveform relations are confirmed by simultaneous superimposed RA/RV pressure recordings (C). Reprinted with permission from reference 9.

View larger version (56K): [in a new window]   Figure 4 Tracings of M pattern of right atrial (RA) pressure. When timed by electrocardiogram (A), most prominent negative deflection in right atrium is coincident with T-wave, suggesting a diastolic Y descent. In contrast, its relation to right ventricular (RV) pressure (B) demonstrates that this prominent descent coincides with peak RV systolic pressure (RVSP), indicating a systolic X descent, whereas diastolic Y descent is blunted. M pattern comprises a depressed A-wave, D descent before a small C-wave, a prominent X descent, a small V-wave, and a blunted Y descent. Peak RVSP is depressed and bifid (arrow) with delayed relaxation and an elevated end-diastolic pressure. (All pressures are measured in mm Hg). Reprinted with permission from reference 9.