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Biomedical subjects

J N Cohn

Publications and source records attributed to J N Cohn.

At least 289 records · Page 16Linked to original sources
PubMed1982

Angiotensin-converting enzyme inhibition in congestive heart failure: the concept.

Plasma renin activity frequently is increased in patients with congestive heart failure. This increase in inversely related to serum sodium concentration, but is not correlated with hemodynamic measurements. Nonetheless, inhibition of converting enzyme activity by administration of teprotide or captopril results in a decrease in systemic vascular resistance that is directly related to the control plasma renin activity. These data suggest that angiotensin II contributes to the systemic vasoconstriction of heart failure and that chronic inhibition of the renin-angiotensin system may have a salutary effect on left ventricular performance in patients with heart failure.

Angiotensin II↗
PubMed1982

Response of plasma norepinephrine and epinephrine to dynamic exercise in patients with congestive heart failure.

The activity of the sympathetic nervous system is increased at rest in patients with congestive heart failure. To determine whether this augmentation is carried over during dynamic upright exercise, 14 patients with congestive heart failure were stressed maximally during upright bicycle ergometry. Plasma norepinephrine and epinephrine levels were measured in the basal upright (sitting) posture before and during maximal exercise. The results were compared with those in six healthy control subjects before and during maximal exercise. Plasma norepinephrine increased during exercise from a mean (+/- standard error of the mean) of 650 +/- 95 to 1,721 +/- pg/ml in the group with heart failure. This increase was significantly less (p less than 0.001) than that in the control group (from 318 +/- 36 to 3,230 +/- 418 pg/ml). However, for equivalent levels of total body oxygen consumption (VO2), the group with heart failure had higher levels of plasma norepinephrine than the control group. Plasma epinephrine was similar in the two groups in the basal upright position (92 +/- 18 and 92 +/- 26 pg/ml), but it increased more during exercise in the normal subjects (743 +/- 210 pg/ml) than in the group with heart failure (167 +/- 67 pg/ml) (p less than 0.001). The percent increase in norepinephrine correlated with the percent change in VO2 in the group with heart failure (r = 0.62, p less than 0.02), but the percent change in epinephrine did not. There is, therefore, a disturbance in the sympathetic nervous system during exercise in patients with congestive heart failure. Although norepinephrine increases in such patients to a greater extent than in normal subjects at lower levels of exercise, the extremely high levels of norepinephrine and epinephrine generated by normal subjects during maximal upright exercise do not occur in patients with heart failure.

Adult↗
PubMed1982

Relationship of exercise capacity to resting left ventricular performance and basal plasma norepinephrine levels in patients with congestive heart failure.

Seventeen patients with chronic congestive heart failure (CHF) were studied to assess the relationship of resting left ventricular function, as measured by noninvasive and invasive methods, to maximal exercise capacity, as measured by peak total body oxygen consumption (VO2). Supine basal plasma norepinephrine (NE) was also measured to evaluate its relationship to the severity of heart failure and to determine whether it may be a better predictor of exercise capacity in patients with CHF than the more commonly employed noninvasive and invasive tests of left ventricular function. Fourteen of the 17 patients underwent upright bicycle exercise (average peak VO2 10.60 +/- 1.40 ml/kg/min, +/- SEM) to their symptomatic maximum. There was no significant correlation between peak VO2 and the noninvasive measurements of left ventricular performance obtained at rest, including cardiothoracic ratio, left ventricular internal dimension by M-mode echo, percent shortening of the minor axis by M-mode echo, and radionuclide ejection fraction. Hemodynamic measurements were performed in 16 patients. The hemodynamic measurements at rest also failed to correlate with exercise capacity. The supine basal plasma NE, which was elevated in these 17 patients (612 +/- 100 pg/ml), had an inverse relationship with stroke work index (r - -0.70, p less than 0.01) and stroke index (r = -0.83, p less than 0.001) and a positive correlation with right atrial pressure (r = 0.81, p less than 0.001). Although both noninvasive and invasive measurements at rest failed to correlate significantly with peak VO2 during exercise, the plasma NE had a significant inverse correlation with peak exercise VO2 (r = -0.50, p less than 0.05). The basal supine plasma NE is therefore elevated in patients with CHF, is a marker for the severity of CHF as measured by hemodynamics performed at rest, and is a better predictor of exercise capacity than standard noninvasive and invasive tests performed at rest.

Adult↗
PubMed1982

Determinants of acute and long-term response to converting enzyme inhibitors in congestive heart failure.

In 42 patients with moderate-to-severe congestive heart failure (CHF), the acute hemodynamic and neurohumoral response to the converting enzyme inhibitors (CEIs) captopril (CPT) and teprotide were measured. Plasma renin activity (PRA) was elevated and correlated with control plasma norepinephrine (PNE) but not with any of the control hemodynamics. Acutely after CEIs, significant (p less than 0.001) decreases in right atrial pressure, pulmonary artery pressure (PAP), capillary wedge pressure (PCWP), mean arterial pressure (MAP), total systemic vascular resistance (SVR), pulmonary vascular resistance (PVR), and heart rate (HR, p less than 0.002), as well as an increase in cardiac index (p less than 0.001), were observed. Control PRA correlated with the degree of hemodynamic change for PAP (r = -0.64), PCWP (r = -0.66), SVR (r = -0.61), and PVR (r = -0.61). Long-term CPT therapy in 12 of these patients resulted in symptomatic improvement and a marked increase in exercise tolerance (7.4 to 10.4 minutes, p less than 0.009). These data suggest that CEIs effect beneficial acute hemodynamic improvements in depressed left ventricular function, leading to substantial reduction in disabling symptomatology and augmentation of exercise capacity in patients with stable severe CHF. Thus, CPT appears to provide well-tolerated, effective long-term ambulatory vasodilator therapy for advanced cardiac dysfunction.

Adult↗
PubMed1982

Hydralazine in the long-term treatment of chronic heart failure: lack of difference from placebo.

Although hydralazine improves cardiac performance in patients with chronic left ventricular failure, its long-term clinical efficacy has not been established in controlled trials. We carried out a double-blind randomized trial of hydralazine (200 mg daily in 16 patients) versus placebo (16 patients) in patients with class III and IV symptoms while they were taking digitalis and diuretics. Maximal treadmill exercise time was determined prior to and at 4, 10, 18, and 26 weeks of hydralazine or placebo treatment; average follow-up was 20 weeks. We found no change in body weight, clinical class, resting heart rate and blood pressure, or heart size (by chest x-ray examination and echocardiogram) during treatment in either group. The total number of complicating clinical events was insignificantly fewer in the hydralazine treated group (8 vs 13). Control exercise duration in the hydralazine group averaged 259 +/- 21 seconds (SEM), and increased to 347 +/- 35 seconds at 4 weeks (p less than 0.01) and 421 +/- 38 seconds at 26 weeks (p less than 0.001). Exercise duration also increased significantly in the placebo group, from 271 +/- 30 seconds at control to 340 +/- 44 seconds at 4 weeks (p less than 0.02) and 339 +/- 46 seconds at 26 weeks (p less than 0.02). No differences between groups were significant. Left ventricular ejection fraction remained depressed and unchanged in both groups. Thus long-term vasodilator treatment with hydralazine alone is not significantly more effective than placebo in chronic heart failure.

Adult↗
PubMed1982

Vasodilator therapy: implications in acute myocardial infarction and congestive heart failure.

The physiologic effects of systemic vasoconstriction on left ventricular performance and the salutary hemodynamic effect of acute administration of vasodilator drugs to patients with heart failure provide a rational basis for vasodilator therapy in acute myocardial infarction and chronic congestive heart failure. Use of vasodilators during the acute phase of myocardial infarction may reduce mortality when left ventricular filling pressure remains markedly elevated for at least 8 hours after the onset of clinical syndrome. Use of chronic vasodilator therapy in patients with congestive heart failure appears to have been effective in some patients in prolonging exercise tolerance; however, the likelihood of a beneficial effect and the impact of this therapy on the natural history of the disease remain unclear. A Veterans Administration Cooperative Study to address these questions is currently in progress. The new effort directed to studying the effects of vasodilator drugs in these syndromes has appropriately focused attention on their pathophysiology and natural history.

Clinical Trials as Topic↗
PubMed1982

A review of the haemodynamic effects of labetalol in man.

1 Labetalol at a dose of 800 to 1600 mg daily inhibited isoprenaline-induced tachycardia and phenylephrine-induced elevation in arterial pressure in hypertensive subjects. The beta-adrenoreceptor effect was four times more potent than the alpha-adrenoreceptor effect. 2 Isoprenaline-induced tachycardia was more effectively blocked than isoprenaline-induced inotropism, thereby raising the possibility of a subselective effect on cardiac beta-adrenoceptors. 3 Labetalol reduced blood pressure in hypertensive subjects with no change in cardiac output in the supine or upright position and with marked inhibition of the heart rate and blood pressure response to treadmill exercise. 4 Labetalol administered in single doses to patients with stable, treated congestive heart failure impaired blood pressure support during exercise. 5 The unique adrenoceptor and haemodynamic effects of labetalol make it a potentially attractive drug for management of hypertension and other cardiovascular disorders.

Blood Pressure↗
PubMed1982

Hyponatraemia as a marker for high renin heart failure.

The factors that might activate the renin-angiotensin system in treated heart failure were explored. Serum Na+ correlated inversely with plasma renin activity. The degree of congestive heart failure measured by right atrial pressure, pulmonary capillary wedge pressure, cardiac index, and systemic vascular resistance did not correlate with plasma renin activity. Similarly, renal function as measured by blood urea nitrogen, creatinine, and urinary Na+ excretion did not correlate with plasma renin activity. In a prospectively screened group, seven patients with congestive heart failure who were found to be hyponatraemic had plasma renin activities greater than 15 ng/ml per h. Serial determinations in one patient showed plasma renin activity to vary inversely with the serum Na+. It is concluded that serum sodium can be used to identify those patients with congestive heart failure who have a high plasma renin activity. The value of identifying these high renin heart failure patients was seen in their response in four cases to specific therapy with a converting enzyme inhibitor.

Captopril↗
PubMed1982

Response of vasopressin and norepinephrine to lower body negative pressure in humans.

To examine the contributions of cardiopulmonary and sinoaortic baroreceptors to the nonosmotic release of arginine vasopressin (AVP) in normal humans, we subjected nine individuals without evidence of hypertension or heart disease to graded, lower body negative pressure (LBNP). We also studied the effects of this maneuver on sympathetic nervous system activity using plasma norepinephrine (NE) as an index. Heart rate (HR), mean arterial pressure (MAP), pulse pressure (PP), and central venous pressure (CVP) were measured in the control state and during two consecutive levels of increasingly intense LBNP. At each stage blood was sampled for AVP and NE. AVP was analyzed by radioimmunoassay, NE by a radioenzymatic method. During the first level of LBNP, CVP decreased with no change in HR, MAP, or PP. NE increased from 147 +/- 47 to 212 +/- 53 (SD) pg/ml, P less than 0.01, whereas AVP (5.0 +/- 1.0 pg/ml) did not change. With increased suction CVP fell further, HR increased, and PP narrowed, but MAP did not change. NE further increased to 291 +/- 58 pg/ml (P less than 0.01), but AVP still did not change significantly. One subject became markedly hypotensive, and his AVP increased from 2.6 to 81 pg/ml. A fall in CVP that results in sympathetic activation presumably via cardiopulmonary receptors does not therefore increase AVP levels; a further fall in CVP that leads to modest unloading of the sinoaortic baroreceptor and further increased sympathetic activity also fails to stimulate AVP. Hypotension, however, is accompanied by a rapid and profound increase in circulating AVP.

Arginine Vasopressin↗
PubMed1982

Echocardiographic assessment of left ventricular hypertrophy and function in renal hypertensive dogs.

To investigate the performance of the hypertrophied left ventricle, M-mode echocardiographic measurements were performed 2 to 3 times weekly on 8 unanesthetized dogs for several weeks before and for 6 months after the induction of perinephritic hypertension. Four dogs with sham-wrapping and contralateral nephrectomy served as the controls. From a baseline value of 7.7 +/- 0.4 mm (mean +/- SD), left ventricular wall thickness increased to 9.0 +/- 0.6 mm (p less than 0.001) by the 4th week after the induction of hypertension and reached a plateau of 10.2 +/- 1.2 mm (p less than 0.001) by week 10. Fractional shortening of left ventricular dimension (% delta D) increased during early left ventricular hypertrophy and remained elevated for 6 months in the surviving 6 hypertensive dogs. In hypertensive dogs, left ventricular concentric hypertrophy became detectable by week 6 of hypertension. Control dogs did not show these changes. At autopsy, the left ventricular weight of hypertensive and normotensive control dogs was (6.2 +/- 1.4 g/kg and 4.3 +/- 0.5 g/kg (p less than 0.05). In summary, during the early stage of left ventricular hypertrophy in renal hypertensive dogs cardiac performance increased. There is no evidence for deterioration of left ventricular performance as concentric left ventricular hypertrophy develops and becomes chronic.

Animals↗
PubMed1981

An interdisciplinary comparison of consultation outcomes. Psychiatry vs cardiology.

Responses to cardiologists' and psychiatrists' recommendations for drugs and diagnostic actions were compared in a retrospective study of 788 consultations. Variables significantly related to outcome achieved by cardiologists and psychiatrists were identified; similarities among these variables were evident only for the drug recommendations. Cardiologists' recommendations achieved a higher rate of concordance than psychiatrists' for both drugs and diagnostic actions. For drug recommendations, the interservice discrepancy in concordance was directly related to differences in timing of the consultations and incidence of recommendations to start a drug. For diagnostic recommendations, however, the difference was directly related to the consultants' service. The following factors may explain the less favorable outcome for psychiatrists' diagnostic recommendations: (1) the reasons for seeking psychiatric consultation, (2) the consultees' expectations, and (3) the skill of the psychiatrists in offering these recommendations.

Cardiology↗