To investigate coupling between the heart and arterial system in normal subjects and cardiac patients, we determined both the slope of the left ventricular end-systolic pressure-volume relation (ventricular elastance) and the slope of the arterial end-systolic pressure-stroke volume relation (effective arterial elastance) in three groups of subjects: group A, 12 subjects with ejection fraction of 60% or more; group B, seven patients with ejection fraction of 40-59%; and group C, nine patients with ejection fraction of less than 40%. We also determined the left ventricular stroke work, end-systolic potential energy, and the ventricular work efficiency defined as stroke work per pressure-volume area (stroke work + potential energy). In group A, ventricular elastance was nearly twice as large as arterial elastance. This is a condition for a maximal mechanical efficiency. In group B, ventricular elastance was almost equal to arterial elastance. This is a condition for maximal stroke work from a given end-diastolic volume. In group C, ventricular elastance was less than one half of arterial elastance, which resulted in increased potential energy and decreased work efficiency. Thus, the present study suggests that ventriculoarterial coupling is normally set toward higher left ventricular work efficiency, whereas in patients with moderate cardiac dysfunction, ventricular and arterial properties are so matched as to maximize stroke work at the expense of the work efficiency. Neither the stroke work nor the work efficiency is near maximum for patients with severe cardiac dysfunction.

Background-Sympathoexcitation and respiratory instability are closely related to worsening of chronic heart failure. To elucidate the dynamic nature of respiratory modulation of sympathetic activity in patients with heart failure, we studied within-breath variation of muscle sympathetic nerve activity (MSNA) under various ventilatory volumes. Methods and Results-MSNA, blood pressure, and respiratory flow were recorded in 23 patients with left ventricular ejection fraction Յ45%. Within-breath suppression of MSNA (neural silence) was found in 11 patients (MSNA bursts: 71Ϯ10/100 heartbeats) but not in the remaining 12 patients (MSNA bursts: 88Ϯ8/100 heartbeats). Patients without neural silence had a smaller tidal volume (391Ϯ70 versus 267Ϯ75 mL/m 2 , PϽ0.01) and a higher respiratory rate (15Ϯ2 versus 19Ϯ4 breaths/min, PϽ0.01) during spontaneous respiration than those with neural silence. The relationship between tidal volume and minimal amplitude of MSNA bursts in each breath was obtained during random-interval breathing and fitted by an exponential function. The curve of patients without neural silence was shifted to the right and upward, which suggests that a greater tidal volume was required to suppress MSNA (227Ϯ70 versus 437Ϯ195 mL/m 2 , PϽ0.01). Conclusions-Sympathoexcitation in patients with chronic heart failure is closely related to both a decrease in resting tidal volume and an attenuated sympathoinhibitory effect of lung inflation reflex.

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To elucidate the time course of sympathovagal balance and its relationship to left ventricular function in heart failure, we serially evaluated left ventricular contractility and relaxation and autonomic tone in 11 conscious dogs with tachycardia-induced heart failure. We determined a dynamic map of sympathetic and parasympathetic modulation by power spectral analysis of heart rate variability. The left ventricular peak +dP/dt substantially fell from 3,364 +/- 338 to 1,959 +/- 318 mmHg/s (P < 0.05) on the third day and declined gradually to 1,783 +/- 312 mmHg/s at 2 wk of rapid ventricular pacing. In contrast, the time constant of left ventricular pressure decay and end-diastolic pressure increased gradually from 25 +/- 4 to 47 +/- 5 ms (P < 0.05) and from 10 +/- 2 to 21 +/- 3 mmHg (P < 0.05), respectively, at 2 wk of pacing. The high-frequency component (0.15-1.0 Hz), a marker of parasympathetic modulation, decreased from 1,928 +/- 1,914 to 62 +/- 68 x 10(3) ms2 (P < 0.05) on the third day and further to 9 +/- 12 x 10(3) ms2 (P < 0.05) at 2 wk. Similar to the time course of left ventricular diastolic dysfunction, plasma norepinephrine levels and the ratio of low (0.05- to 0.15-Hz)- to high-frequency component increased progressively from 135 +/- 50 to 532 +/- 186 pg/ml (P < 0.05) and from 0.06 +/- 0.06 to 1.12 +/- 1.01 (P < 0.05), respectively, at 2 wk of pacing. These cardiac and autonomic dysfunctions recovered gradually toward the normal values at 2 wk after cessation of pacing. Thus a parallel decline in left ventricular contractility with parasympathetic influence and a parallel progression in left ventricular diastolic dysfunction with sympathoexcitation suggest a close relationship between cardiac dysfunction and autonomic dysregulation during development of heart failure.

The effect of preexistent coronary collateral perfusion on the prevention of left ventricular aneurysm formation was examined in 47 patients undergoing an intracoronary thrombolysis within 6 hours after the onset of a first acute anterior myocardial infarction. Left ventricular aneurysm formation and wall motion were analyzed with cineventriculography. A left ventricular aneurysm was determined as well-defined demarcation of the infarcted segment from normally contracting myocardium. In 25 patients with successful thrombolysis (group A), a left ventricular aneurysm was observed in one patient (4%) during the chronic stage of infarction. In 10 patients who had a significant collateral circulation to the infarct-related coronary artery and unsuccessful reperfusion (group B), the left ventricular aneurysm was observed in only one patient (10%). In the remaining 12 patients with unsuccessful recanalization in the absence of a significant collateral perfusion (group C), there was a higher incidence (seven of 12, 58%) of left ventricular aneurysm formation than in groups A and B (p <0.05). In group A, both the global ejection fraction and regional wall motion in the infarct areas improved significantly (p< 0.05) between the acute and chronic stages of infarction. By contrast, in groups B and C, these indexes on the ventricular function did not change significantly during the convalescent period. Thus, although the collateral perfusion existing at the onset of acute myocardial infarction may not improve ventricular function, it exerts a beneficial effect on the prevention of left ventricular aneurysm formation. (Circulation 1989;79:791-796) It is generally accepted that early recanalization of an infarct-related coronary artery in the presence of residual flow resulting from either a subtotal obstruction of infarct-related coronary artery or collateral perfusion exerts a beneficial effect on the regional and global left ventricular wall motion evaluated during the chronic stage of infarction.1-3 However, it is still controversial whether a preexistent coronary collateral circulation contributes to the preservation of jeopardized myocardial function in the case of unsuccessful recanalization. The purpose of our study was to evaluate the relation of significant collateral perfusion to regional myocardial function and left ventricular aneurysm formation in patients with acute myocardial infarction who were treated with intracoronary thrombolysis. Methods Study PatientsOver a 4-year period, 47 consecutive patients with a first acute anterior myocardial infarction who had complete occlusion of the proximal part of the left anterior descending coronary artery were referred for intracoronary thrombolysis during the first 6 hours after the onset of symptoms. There were 39 men and eight women with a mean age of 60 years (range, 35-79). The diagnosis of acute myocardial infarction included the presence of persistent ST segment elevation of 2 mm or greater in two or more leads on the standard 12-lead electrocardiogram and seve...

The purpose of the present study was to investigate the effects of long-term renal denervation (RD) on heart failure due to myocardial infarction (MI). Wistar rats were anesthetized and the bilateral renal nerves were surgically denervated 2 days before MI was induced by coronary artery ligation. Four weeks later, left ventricular (LV) function and sodium excretion were determined. In MI rats, RD improved the reduced sodium excretion. MI + RD rats revealed lower LV end-diastolic pressure and greater maximum dP/dt as compared with those of MI+ innervation (INN) rats. LV end-diastolic and end-systolic dimensions were significantly smaller and LV fractional shortening was greater in MI + RD rats than in MI + INN rats (20.9% +/- 3.2% vs 14.9% +/- 3.0%). In rats without MI, RD did not affect either sodium excretion or LV function and dimensions. The present results suggest that the long-term RD reduces LV filling pressure and improves LV function after MI, probably due to a restoration of impaired natriuresis. Increased renal sympathetic nerve activity might contribute to the progression of heart failure after MI.

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on behalf of the J-RHYTHM Registry Investigators* Background--To clarify the influence of hypertension and blood pressure (BP) control on thromboembolism and major hemorrhage in patients with nonvalvular atrial fibrillation, a post hoc analysis of the J-RHYTHM Registry was performed.