SUMMARY The linearity and sensitivity of the end-systolic pressure-volume (P-Ve,) relation to the inotropic state of the left ventricle were investigated in 11 patients with coronary heart disease and one patient with congestive cardiomyopathy. To minimize autonomic reflex responses, propranolol, 0.15 mg/kg, and atropine, 1 mg, were administered i.v. at the beginning of the study. Three ventriculograms were performed: at rest, after oral isosorbide dinitrate, 10 mg (systolic pressure decrease 15 mm Hg), and during infusion of methoxamine, 2 mg/min (systolic pressure increase > 10 mm Hg).The three points of the P-Ve, relation showed linearity (r 0.96). The relation between the slope k of the PVe, relation and the left ventricular ejection fraction at rest was best described by an exponential function (r = 0.94). The use of peak systolic pressure instead of end-systolic pressure showed equally good results. The intercept of the P-V,, line on the abscissa, which represents the theoretical end-systolic volume at zero pressure, was not related to the ejection fraction under control conditions. The P-Ve, relation in postextrasystolic beats was displaced toward the left (smaller end-systolic volumes) and became steeper.MYOCARDIAL fiber shortening is determined by preload, afterload and contractility, and end-systolic fiber length is inversely proportional to afterload.' In the isolated left ventricle, end-systolic fiber length is linearly related to end-systolic tension.2 In the experimental animal, the isolated left ventricle also shows a linear end-systolic pressure-volume (P-Ves) relationship that is not dependent on preload. The slope of the P-Ve, relation is determined by the contractile state and is increased by positive inotropic interventions.3Although the concept of the P-Ve, relationship has been applied for some time in animal experiments,1-4only recently has the P-Ve, relation been investigated as a means of assessing left ventricular function in man.Our study was undertaken to determine (1) whether the P-VVe, relation in man is linear; (2) the correlation between the slope k of the P-V,e relation and other variables of left ventricular function; (3) whether the theoretical volume at zero pressure (VO), i.e., the intercept of the P-Ves relation on the abscissa, reliably separates impaired from normal left ventricular func-

No abstract

In the past, cardiac changes in renal failure have commonly been ascribed to hypertension and poorly specified toxic effects ('uraemic cardiomyopathy'). Our recent experimental and clinical studies suggest (a) that cardiac hypertrophy can be dissociated from hypertension and that blood pressures may have only a permissive role, (b) that experimental uraemia is associated with specific activation of pericytes and intermyocardiocytic fibrosis. Cardiac hypertrophy not correlated with elevated blood pressure, and intermyocardiocytic fibrosis not observed in similarly hypertensive non-uraemic patients, have recently been documented in dialysis patients. The implications of these findings may be (a) electrical instability and predisposition to a sudden cardiac death and (b) diastolic cardiac malfunction with impaired LV filling and predisposition to dialysis hypotension. Some evidence for the latter possibility is provided.

We used Doppler echocardiographic techniques firstly to examine left ventricular (LV) filling patterns in dialysis patients, secondly to analyse whether Doppler echocardiographic left ventricular filling pattern is different in patients with recurrent intradialytic hypotension, and thirdly to study the relation between blood pressure decrease during volume subtraction and left ventricular filling pattern. Indices of left ventricular filling patterns of 47 dialysis patients were consistently different when compared to normotensive healthy controls. To further assess the relation of left ventricular filling pattern to blood pressure stability on dialysis, we first compared 24 patients with stable intradialytic blood pressure (BP) and 23 patients with one or more episodes or intradialytic hypotension per month. Patients with recurrent intradialytic hypotension had lower predialysis blood pressure (MAP 89 +/- 13 vs 96 +/- 14 mmHg), more severe concentric hypertrophy (left ventricular mass/volume ratio 2.7 +/- 1.4 vs 2.0 +/- 0.7), and impaired left ventricular filling (Doppler) as indicated by the ratio of early diastolic vs late (atrial) filling (0.66 +/- 0.2 vs 0.95 +/- 0.22). Subsequently we assessed by Doppler technique the effect of a predetermined rate of volume subtraction (during one dialysis session) in patients with or without recurrent intradialytic hypotension. Diastolic filling indices deteriorated consistently prior to the reduction in blood pressure (early diastolic filling 26.8 +/- 15.2 vs 45.4 +/- 10.9% of diastolic filling). It is suggested that impaired left ventricular filling, presumably reflecting disturbed left ventricular compliance, is common in dialysis patients. Findings by noninvasive Doppler techniques suggest a role of abnormal left ventricular distensibility in recurrent dialysis hypotension.

We studied the effect of bilateral common carotid occlusion (implanted pneumatic cuffs) on renal blood flow (electromagnetic flowmeter) and renal function (implanted ureteral catheter) in nine chronically instrumented, conscious dogs on a high sodium diet (14 mmol/kg body weight per day). By means of suprarenal aortic constriction (pneumatic cuff) the influence of renal perfusion pressure was investigated. There was no change in renal blood flow or glomerular filtration rate (inulin clearance) with either reflexly increasing (+49.6%) or constant renal perfusion pressure. Carotid occlusion caused an increase of urine output by 80.5% and of sodium excretion by 85.3% due to a fall in fractional sodium reabsorption (-0.9%) when renal perfusion pressure was allowed to rise. Neither an increase of diuresis or sodium excretion nor an antinatriuresis was observed when renal perfusion pressure was kept constant during carotid occlusion. We conclude that, in conscious dogs at rest, the moderate sympathetic activation associated with carotid occlusion is too small to induce renal sympathetic vasoconstriction or antinatriuresis. The "carotid sinus polyuria" is a pressure-diuresis.