Carotid artery distensibility and distending pressure in hypertensive humans.

Whether the decrease in large-artery distensibility observed in hypertensive patients is due primarily to an increase in distending pressure or to hypertension-induced changes in structural properties has been much debated. We determined noninvasively the diameter-pressure curve of the common carotid artery over the systolic-diastolic range by continuously recording both the pulsatile changes in internal diameter (high-resolution echo-tracking system) and, simultaneously on the contralateral artery, the pressure waveform (high-fidelity applanation tonometry). We then derived the distensibility/pressure curve and compared arterial distensibility in 14 normotensive subjects and 15 age- and sex-matched hypertensive subjects at their respective mean arterial pressures (MAP) and at a common distending pressure: 100 mm Hg. Distensibility decreased as blood pressure increased, and distensibility at MAP was significantly lower in hypertensive than in normotensive subjects (7.8 +/- 0.7 versus 11.7 +/- 1.7 kPa-1.10(-3), mean +/- SEM; P < .05). In hypertensive subjects, the distensibility-pressure curve was shifted toward higher levels of blood pressure, and a large part of the curve overlapped that of normotensive subjects. No significant downward shift of the distensibility-pressure curve was observed in hypertensive subjects, and distensibility at 100 mm Hg was not significantly different from that of normotensive subjects (10.0 +/- 1.0 versus 9.0 +/- 1.1 kPa-1.10(-3)). Distensibility at 100 mm Hg decreased with aging (P < .05) and was not reduced in hypertensive subjects compared with normotensive subjects after adjustment for age.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular-arterial coupling in systemic hypertension: analysis by means of arterial effective and left ventricular elastances.

OBJECTIVE: To clarify the spectrum of the left ventricular responses in hypertension in man by means of coupled analysis of elastances. In the present study we analysed the 'functional' coupling of the left ventricle and the arterial system in terms of the arterial effective elastance (E(a)) divided by a value of end-systolic left ventricular elastance approximated by the end-systolic pressure-volume ratio (E(lv)). METHODS: Twenty-five normotensive and 19 hypertensive males without heart failure underwent a haemodynamic and angiographic study. The hypertensives were divided into three subgroups: group 1 had normal ejection fraction, group 2 had ejection fraction > 70% and group 3 had ejection fraction 50-58%. RESULTS: The ejection fraction was similar in hypertensives and controls and E(lv) was significantly increased in the hypertensives. E(a) was identical in the three hypertensive subgroups, which differed only for E(lv). Hypertensives with a normal ejection fraction (n = 8) had a normal E(a)/E(lv) ratio and end-systolic stress, and a significantly increased E(lv), related mainly to an increase in the left ventricular mass divided by the end-diastolic volume (m/VED) with normal systolic function of the left ventricular muscle. The significantly increased systolic pump function of group 2 (n = 5) seems to be related to a significant increase in both m/VED and left ventricular muscle contractility. Group 3 (n = 6) was more heterogeneous, some patients having insufficient hypertrophy and others impaired muscle function. CONCLUSIONS: The left ventricle and the arterial system remain correctly coupled in hypertensives overall, but with marked heterogeneity of the systolic pump (and sometimes muscle) function and mainly of the geometry of the left ventricle. Regarding the relatively unequivocal changes in Ea, the differences in ejection fraction and in left ventricular-arterial coupling in hypertensives are related mainly to changes in the left ventricular systolic pump function.

Serial assessment of cardiopulmonary exercise capacity after cardiomyoplasty for either ischemic or idiopathic dilated cardiomyopathy.

Cardiomyoplasty is a surgical procedure aimed at assisting the left ventricle during ejection. We describe the long-term effects of cardiomyoplasty on peak exercise capacity, with serial assessments for up to 3 years after operation. Sixteen patients (12 in New York Heart Association class III and 4 in class IV) were enrolled. The mean left ventricular ejection fraction was 18 +/- 8%. Bicycle exercise tests with respiratory gas analysis were performed preoperatively and 6, 12, 18, 24, and 36 months after operation. Mean follow-up was 12 +/- 5 months (range 6 to 24). At 6 months, peak oxygen consumption and the ventilatory threshold were unchanged (from 17.8 +/- 5.8 to 15.8 +/- 5.3 ml/min/kg, and from 12.1 +/- 2.7 to 11.4 +/- 3.4 ml/min/kg, respectively). Ventilation at 50 W, viewed as an index of polypnea at submaximal exercise, was also unchanged. Serial assessment of exercise capacity thereafter showed no changes. However, ejection fraction tended to increase from 18 +/- 8% to 21 +/- 9% (p=0.08) and 14 patients reported an improvement in their functional status, resulting in a significant change in New York Heart Association functional class (3.3 +/- 0.5 to 2.2 +/- 0.4 at 6 months and 2.4 +/- 0.4 at the last visit, p <0.005) and improvement in quality-of-life scores. Thus, cardiomyoplasty does not appear to increase peak exercise capacity in the long term, despite an improvement in the left ventricular ejection fraction. Symptoms and quality of life, however, appear to improve. This may be related in part to an insufficient number of assisted systoles during exercise, persistent deconditioning, or changes in pulmonary mechanics.

Effects of aging on left ventricular-arterial coupling in man: assessment by means of arterial effective and left ventricular elastances.

The ejection fraction (EF) is a load-dependent index of the systolic function of the left ventricle (LV), which depends on the 'functional' coupling of the LV with the arterial system, evaluated by the ratio between arterial effective elastance (Ea) to end-systolic left ventricular elastance. The spectrum of changes in LV and the arterial system during aging has not been studied by means of coupled analysis of elastances. Twenty-five normotensive healthy subjects aged from 22 to 68 years underwent hemodynamic and angiographic studies. The functional properties of the arterial system were evaluated in terms of Ea (end-systolic pressure/stroke volume), and the systolic function of the LV was approximated by the end-systolic pressure to end-systolic volume ratio (Elv). The result is that Ea increased linearly with age. Elv increased less than Ea. The positive relationship between Ea/Elv and age was close to statistical significance (r = 0.39, p = 0.07), suggesting that left ventricular-arterial coupling changes little with aging. Analysis of the relationship between EF and end-systolic stress showed that several points were situated at the lower part of the relationship in elderly subjects, suggesting a decrease in the intrinsic contractility of left ventricular muscle in some cases. Aging is characterized by a simultaneous increase in arterial system elastance and the systolic performance of the left ventricular pump, thereby preserving the transfer function of the arterial system as a whole. However, some aged subjects may depart from this rule, probably because of variability in the capacity to produce myocardial hypertrophy and/or altered inotropy of the muscle.

Small abnormal echos after mitral valve replacement with bileaflet mechanical prostheses: predisposing factors and effect on thromboembolism.

Early transesophageal echocardiography (TEE) after mitral valve replacement can detect symptomless, non-obstructive thrombus on prosthetic valves and also small filamentous abnormal echoes (SAE). The object of this study is to evaluate their respective frequency and predisposing factors. Between October 1988 and June 1992, 129 consecutive patients underwent mitral valve replacement with a bileaflet prosthesis and had transesophageal echocardiography at an average of 15 +/- 7 days (range: 6-35 days) after surgery. Details of postoperative anticoagulation were analyzed in 99 patients from five surgical centers having comparable postoperative anticoagulation protocols. Among those patients presenting with SAE, 76% had a second transesophageal echocardiography at an average of 145 +/- 166 days after the first examination. Mean age was 56 +/- 13 years. Small filamentous echoes were found in 55 patients (43%). In univariate analysis, independent predictors were age, absence of systolic regurgitation across the mitral prosthesis as observed with continuous Doppler, and the presence of spontaneous echo contrast (SC) in the left atrium: 54 +/- 14 years in the absence vs. 59 +/- 10 in the presence of SAE (p < 0.05); 54% of systolic leak vs. 36% (p < 0.05); 43% of SC vs. 75% (p < 0.00001). In multivariate analysis, spontaneous echo contrast was the only independent predictor for SAE (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

[Critical analysis of scales of quality of life in cardiology; applications to cardiac insufficiency]. / Analyse critique des échelles de qualité de vie en cardiologie; applications à l'insuffisance cardiaque.

Scales of quality of life have only recently been imposed in cardiology. Essentially an Anglosaxon invention, they have been used for evaluating most treatment of cardiac failure. The main qualities of a good quality of life questionnaire are its sensitivity, its reproducibility and its validity. The contents of the questionnaire, particularly the relationship between items concerning symptoms and those concerning the psychological aspects of the disease, have a great influence on the quality of results. The "Living with Heart Failure Questionnaire" of the University of Minnesota is the most validated questionnaire at present. As with most other methods of therapeutic assessment in cardiology, the most recently obtained results from large multicenter trials, seem to show a much smaller benefit of drugs reputed to be effective in this condition, with respect to the quality of life of patients. This justifies: the continuation of validation of these questionnaires, a reflection on the efficacy of classical management of these patients.

[Abnormal peripheral circulation in heart failure]. / Anomalies de la circulation périphérique dans l'insuffisance cardiaque.

Left ventricular failure leads to circulatory failure which causes clinical symptoms and in which regional blood flow changes play an important role. An abnormality of systemic vasodilatation on exercise or on pharmacological intervention has been shown. This affects both the resistance and conductive vessels and is mainly functional, related to neurohormonal stimulation with a predominance of vasoconstrictive factors amongst which increased adrenergic tone probably plays an essential part. A modification of the endothelium-dependent response has recently been confirmed. The presence of structural vascular abnormalities (increase in parietal sodium and water concentrations, "remodelling" remains debatable in the human. These abnormalities have a common factor in their chronicity and take time to regress with medical treatment or after cardiac transplantation. Physical training seems to induce more marked and, above all, more rapid effects.

[Arterial compliance is not diminished in hypertensive patients when compared at the same level of blood pressure]. / La compliance artérielle n'est pas diminuée chez l'hypertendu lorsqu'elle est comparée à même niveau de pression artérielle.

Whether the decrease in large artery compliance, observed in hypertensive patients (HT), is due to an increase in distending pressure or to intrinsic alterations of the vascular wall remains much debated. We determined the diameter-pressure curve of the common carotid artery over the systolic-diastolic range, then derived the compliance-pressure curve, in order to compare arterial compliance in normotensive subject (NT) and in HT, for a common level of distending blood pressure: 100 mmHg (isobaric compliance). Fourteen NT and 15 never treated essential HT were included in the study. The diameter-pressure curve of the common carotid artery was determined non-invasively by simultaneously and continuously recording the systolic-diastolic changes in internal diameter (using a high resolution echotracking system) and pressure waveform (using high fidelity applanation tonometry on the contralateral artery) over 4-6 cardiac cycles. The level of MAP of the carotid pressure waveform was determined electronically and set equal to mean brachial pressure. Compliance-pressure curve was then derived from the pressure-diameter curve in order to determine compliance (C) for any given level of blood pressure, particularly MAP (CMAP) and 100 mmHg (C100). Despite the considerable differences in blood pressure, the compliance-pressure curve of HT was not different from that of NT. CMAP decreased with aging (p < 0.001) and MAP (p < 0.001). According to age, CMAP was reduced in HT as compared to NT (84 +/- 49 vs 116 +/- 52 mm2.mmHg.10(-3) p < 0.01). C100 decreased with aging (p < 0.05) but not with MAP. According to age, C100 was not reduced in hypertensives.(ABSTRACT TRUNCATED AT 250 WORDS)

[Role of digitalis glycosides in the treatment of cardiac failure]. / Place des digitaliques dans le traitement de l'insuffisance cardiaque.

While no doubt has ever been cast on the usefulness of digitalis in cardiac failure with atrial fibrillation and a fast ventricular rate, they are periodically brought into question regarding chronic cardiac failure in sinus rhythm. While they have not been supplanted by new positive inotropic agents, they are in competition with converting enzyme inhibitors. Recent therapeutic trials have shown that digitalis preparations, alone or in association with converting enzyme inhibitors, have beneficial effects on symptoms and exercise duration in patients with symptomatic impaired left ventricular systolic function. While the effects of digitalis preparations on mortality remain unknown, a large North American study should soon provide an answer to this question.

[What is the appropriate treatment for myocardial infarction with left ventricular dysfunction?]. / Quel traitement après un infarctus du myocarde avec dysfonction ventriculaire gauche?

The essential goal of medical treatment following myocardial infarction with left ventricular dysfunction must be the prevention of secondary cardiac failure. The existence of left ventricular dysfunction, in particular when it is not accompanied by clinical cardiac failure, is a virtually formal indication for beta-blocker treatment after an infarction. Beta-blockers with intrinsic sympathomimetic activity (ISA) are possibly better tolerated in this context. However, experience shows that cardiologists and general practitioners often remain reluctant to prescribe beta-blockers whenever left ventricular function is impaired. Converting enzyme inhibitors decrease the risk of onset of secondary cardiac failure, reduce sudden deaths by ventricular arrhythmias, reduce recurrences of myocardial infarction or unstable coronary insufficiency, and more generally reduce overall and cardiovascular mortality. This is a class effect. While there is no urgency to prescribe them during the acute phase, it is generally considered that it is extremely useful to give them fairly quickly, i.e. during the first 72 hours. At the end of the hospital phase, around two weeks, it is desirable, whenever possible, to prescribe a dose of the order of 75 mg/day of captopril or 2.5 mg/day of ramipril. The administration of aspirin can be considered virtually routine. Oral anticoagulants are desirable in the presence of a large akinetic pocket, a frequent starting point of thrombosis and/or systemic emboli, or in the presence of atrial fibrillation. Digitalis/diuretic treatment does not appear to be indicated at this stage. Other types of anti-ischemic treatment are not theoretically indicated as a matter of principle at this stage in the absence of residual ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Prolonged kinetics of recovery of oxygen consumption after maximal graded exercise in patients with chronic heart failure. Analysis with gas exchange measurements and NMR spectroscopy.

BACKGROUND: Patients with chronic heart failure (CHF) often complain of prolonged dyspnea after exercise. The determinants of oxygen consumption after exercise in these patients are unknown. We hypothesized that the kinetics of oxygen consumption recovery after graded exercise was prolonged in parallel with the recovery of muscle energy stores, was not affected by the exercise level, and could be used to assess the circulatory response to exercise. METHODS AND RESULTS: Seventy-two patients with CHF in Weber's class A (n = 28), B (n = 21), and C/D (n = 23) and 13 healthy subjects performed maximal upright bicycle exercise with breath-by-breath respiratory gas analysis. Kinetics of recovery of ventilation (VE), oxygen consumption (VO2), and CO2 production (VCO2) after exercise were characterized by T1/2, the time to reach 50% of the peak value. T1/2 VO2 (seconds) increased with the severity of CHF (97 +/- 17 for CHF A [P < .05 versus CHF B, P < .05 versus CHF C/D], 119 +/- 22 for CHF B [P < .05 versus control subjects, P < .05 versus CHF A, and P < .05 versus CHF C/D], 155 +/- 55 for CHF C/D [P < .05 versus control subjects, P < .05 versus CHF A, and P < .05 versus CHF B] compared with 77 +/- 17 for control subjects). T1/2 VCO2 and T1/2 VE also increased similarly with the worsening of CHF. T1/2 VO2 was correlated negatively with peak VO2 (r = .65) and was reproducible (r = .96). To study the relation between T1/2 VO2 and the duration of exercise, 10 healthy subjects and 22 patients underwent a second graded test at 75% and/or 50% of peak workload. T1/2 VO2 was minimally shortened, at only 50% of peak workload (P = .02). Finally, 19 patients underwent 31P nuclear magnetic resonance spectroscopy of the anterior compartment of the leg during exercise; the half-time of recovery of the ratio of inorganic phosphate to creatine phosphate (T1/2 Pi/PCr), reflecting the level of involvement of oxidative metabolism in the restoration of energetic metabolites after exercise, was linearly correlated with the half-time of VO2 recovery (r = .70, P < .01). CONCLUSIONS: Postexercise T1/2 VO2 increases when CHF worsens, perhaps in part a result of slower kinetics of recovery of muscle energy stores. The time course of oxygen consumption recovery may represent a simple new criterion for measuring the impairment of the circulatory response to exercise in CHF, even submaximal exercise.