Aims: Simultaneous biventricular pacing improves left ventricular (LV) systolic performance in patients with dilated cardiomyopathy and intraventricular conduction delay. We tested the hypothesis that further improvements can be obtained using sequential biventricular pacing by optimizing both atrioventricular and interventricular delays. Methods and results: In 12 patients, LV pressure, right ventricular (RV) pressure and respective rates of change of pressure (dPydt) were acutely measured during biventricular pacing with different atrioventricular and interventricular (VVi) intervals ranging from y60 to q40 ms. The average increase vs. baseline in maximum LV dPydt was higher for sequential than for simultaneous biventricular pacing (VDD mode: 35"20 vs. 29"18%, P-0.01; DDD mode: 38"23 vs. 34"25%, P-0.01), with a minority of patients accounting for most of the difference. The mean optimal VVi was y25"21 ms in VDD mode and y25"26 ms in DDD mode. With these settings, RV dPydt was not significantly different from baseline. QRS shortening was not predictive of LV dPydt increase. Conclusion: A significant increase of LV dPydt with no change in RV dPydt can be obtained by sequential biventricular pacing as compared to simultaneous biventricular pacing. The highest LV dPydt is achieved when LV is stimulated before RV. The hemodynamic advantage might be of clinical significance in selected cases.

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We report a case in which life support for cardiogenic shock was achieved by a nonpulsatile venoarterial bypass, and left ventricular decompression was obtained by a catheter placed percutaneously through the aortic valve into the left ventricle. The blood drained from the left ventricle was pumped into the femoral artery. The normalization of left heart filling pressures allowed the resolution of pulmonary edema, and the patient underwent a successful heart transplantation following 7 days of mechanical cardiocirculatory support.

Experimental coronary occlusion is accompanied by an acute impairment of the baroreceptorheart rate reflex. This study was planned to determine whether this impairment also occurs in humans. In 30 patients admitted to a coronary care unit for an anterior (n = 14) or inferior (n=16) transmural myocardial infarction (MI), we measured 1) the increase in RR interval induced by stimulating carotid baroreceptors through progressive reductions in neck chamber pressure, 2) the increase in RR interval induced by stimulating arterial baroreceptors through intravenous boluses of phenylephrine, and 3) the reduction in RR interval induced by deactivating arterial baroreceptors through intravenous boluses of nitroglycerin. Measurements were performed 49.5 ±2.4 hours (mean± SEM) after the MI. The results were compared with those of five age-matched patients admitted to the coronary care unit for chest pain and found free from ischemic heart disease. The sensitivity of the carotid baroreceptor-heart rate reflex (slope of the linear regression of RR interval over neck pressure changes) was markedly less in MI than in control patients (3.8 ±0.5 vs. 5.9±0.6 msec/mm Hg, p<0.05), the reduction being similar in patients with anterior and inferior MI. This was the case also for the baroreflex sensitivity measured by the phenylephrine and the nitroglycerin methods (slope of the linear regression of RR interval over systolic blood pressure changes). However, 10.2±0.3 days later, the baroreflex sensitivity measured by all three methods increased significantly (p<0.05 or 0.01) and became similar to that of control subjects, which showed no significant change from the early to the late period after admission into the coronary care unit. Thus, MI is accompanied by an acute marked impairment of the baroreceptor control of the heart in humans, and this is the case both for an anterior and an inferior MI. The impairment is largely transient in nature, however, and a clear-cut recovery of the baroreflex can be seen a few days later. (Circulation 1990;81:939-948) E xperimental coronary occlusion or acutely induced damage of the myocardium is followed by an abrupt impairment of the baroreceptor control of the sinus node,1-4 which is still evident several weeks later.3 This is potentially harmful because baroreceptors increase and reduce vagal and sympathetic influences on the heart, respectively, thereby opposing the adverse effects of ischemia on the electrical stability of the myocardium.5-8 In patients with a previous myocardial infarction (MI), the Valsalva maneuver and the administration of vasoactive drugs cause small changes in heart rate.9-12 Furthermore, a recent study from our institution has shown that in some patients, injection of phenylephrine induced somewhat greater bradycardias months as compared with weeks after the occurrence of an MI.13 This suggests that MI impairs the baroreceptor control of heart rate in humans as well as experimentally, but that some recovery later appears.In all human studies, the baroreceptor-heart ra...

AimsPrevious studies investigating the effect of hypoxia on left ventricle focused on its global function, an approach that may not detect a selective dysfunction of subendocardial layers that are most sensitive to an inadequate oxygen supply. In the HIGHCARE study, aimed at exploring the effects of high altitude hypoxia on multiple biological variables and their modulation by an angiotensin receptor blocker, we addressed the effects of hypobaric hypoxia on both systolic and diastolic left ventricular geometry and function, focusing on echocardiographic assessment of left ventricle twist to indirectly examine subendocardial left ventricular systolic function. Methods and resultsIn 39 healthy subjects, physiological and echocardiographic variables, including left ventricular twist and a simplified torsion-to-shortening ratio (sTSR), were recorded at sea level, at 3400 m, and at 5400 m altitude (Mount Everest base camp). Both left ventricular twist and sTSR were greater at 5400 m than at sea level (12.68 vs. 9.68 and 0.285 vs. 0.202, P , 0.05 for both), were linearly related to the reduction in arterial oxygen partial pressure (P , 0.01 for both), and were associated with significant changes in LV dimensions and contractility. No effects of angiotensin receptor blockade were observed on these variables throughout the study. ConclusionOur study, for the first time, demonstrates an increase in left ventricular twist at high altitude in healthy subjects exposed to high altitude hypoxia, suggesting the occurrence of subendocardial systolic dysfunction in such condition.