PubMed Health⌕ Search

Biomedical subjects

B D Nunez

Publications and source records attributed to B D Nunez.

25 records · Page 2Linked to original sources
PubMed1987

Overweight and sudden death. Increased ventricular ectopy in cardiopathy of obesity.

Obesity has been documented to be an independent risk factor for sudden death and other cardiovascular mortality. The present study was designed to monitor and quantify cardiac arrhythmias in obese subjects with and without eccentric left ventricular hypertrophy, who were matched with regard to arterial pressure, age, sex, and height with lean subjects. Prevalence of premature ventricular (but not atrial) contractions was 30 times higher in obese patients with eccentric left ventricular hypertrophy compared with lean subjects. Similarly, obese patients with left ventricular hypertrophy scored higher with regard to the classification of Lown and Wolf than those without left ventricular hypertrophy and lean subjects having the same level of arterial pressure. Patients' class in the Lown and Wolf system correlated with ventricular diastolic diameter and left ventricular mass. Thus, heart enlargement of the eccentric type as a consequence of obesity predisposes to excessive ventricular ectopy. Echocardiographic assessment and electrocardiographic monitoring allow us to identify the patients who are at highest risk of more serious arrhythmias or possibly sudden death and to subject them to the most specific preventive and therapeutic measures.

Adult↗
PubMed1987

Biventricular cardiac hypertrophy in essential hypertension.

Left ventricular hypertrophy (LVH) is the major adaptation of the heart to a prolonged increase in the left ventricular afterload in hypertension. However, the structure and function of the right ventricle have received little attention. The present study was designed to assess right ventricular structural changes in patients with established essential hypertension. To accomplish this, M-mode echocardiograms were obtained from 15 healthy normotensive subjects and 35 patients with essential hypertension-15 with normal left ventricles and 20 with clear-cut echocardiographic evidence of LVH. In comparison with the normotensive subjects, right ventricular wall thickness was increased almost twofold in the hypertensive patients with LVH (7.0 +/- 2.1 mm vs 3.7 +/- 0.8 mm; p less than 0.001); there was a significant, direct correlation between right and left ventricular wall thickness in the entire patient population (r = 0.65; p less than 0.001). Furthermore, the left atrial emptying index was significantly reduced in all patients with hypertension regardless of whether LVH was present (p less than 0.001) and suggests early diastolic functional involvement of the left ventricle in hypertension. We therefore conclude that right ventricular hypertrophy is associated with LVH in patients with hypertension, although the changes of LVH are frequently more obvious to the clinician.

Cardiomegaly↗
PubMed1987

Serum uric acid in renovascular hypertension: reduction following surgical correction.

Mild hyperuricemia in patients with essential hypertension reflects early renal vascular involvement. This report describes a retrospective analysis of 28 patients with unilateral renal arterial disease and hypertension who underwent surgical treatment. Following surgical repair of the arterial lesion: systolic pressure decreased from 188 +/- 25 to 146 +/- 21 mm Hg (p less than 0.001); diastolic pressure decreased from 108 +/- 4 to 87 +/- 6 mm Hg (p less than 0.001), and serum uric acid and creatinine concentrations decreased from 7.0 +/- 1.1 to 6.1 +/- 1.4 mg/dL and from 1.3 +/- 0.3 to 1.0 +/- 0.3 (p less than 0.02 and p less than 0.03, respectively). The reduced serum potassium levels, reflecting hyperaldosteronism, increased after surgical treatment (p less than 0.003). The 28 patients were classified in three groups according to previous therapy: group I (14 patients) had been treated with a centrally active adrenergic agonist or a beta adrenergic receptor blocking agent; group II (7 patients) had been treated with a diuretic, and group III (7 patients) had never received antihypertensive therapy. Serum uric acid concentrations were similar in each of the three groups and decreased significantly in each group after correction of the renal artery stenosis. These data strengthen our previous observations and further suggest that serum uric acid concentration may be useful as an index of renal vascular involvement in hypertension.

Adult↗
PubMed1987

Cardiovascular effects of verapamil in patients with essential hypertension.

The cardiovascular effects of intravenous verapamil and 3 months of oral administration of a slow-release form of verapamil (verapamil-SR) were studied in 10 patients with mild-to-moderate essential hypertension. Intravenous verapamil reduced arterial pressure by 15% (p less than .01) through a fall in total peripheral resistance of 29% (p less than .01); provoked a reflexive rise in heart rate (by 19%, p less than .02), cardiac output (by 74%, p less than .01), and plasma catecholamines; and shifted intravascular volume toward the cardiopulmonary circulation indicating peripheral venoconstriction. Quite in contrast to the immediate effects of the intravenous drug, oral therapy with verapamil-SR for 2 to 3 months lowered arterial pressure effectively (by 15%, p less than .01) by inducing vasodilation of 15% (p less than .02), but without causing reflex tachycardia, activation of the sympathetic-adrenergic or renin-angiotensin systems, or volume expansion. Oral therapy with verapamil-SR preserved systemic and renal blood flow and slightly reduced cardiac mass (by 6%, p less than .05) and renal vascular resistance (by 25%, p less than .05). Whereas intravenous verapamil tended to depress myocardial contractility, oral verapamil-SR did not at all affect myocardial contractility or left ventricular function. These cardiovascular effects make verapamil-SR an excellent agent for long-term antihypertensive therapy.

Administration, Oral↗
PubMed1987

Disparate cardiovascular findings in men and women with essential hypertension.

We measured systemic hemodynamic, volume, and endocrine findings in 100 hypertensive women matched to 100 men by mean arterial pressure, age, race, and body surface area. Women had a higher resting heart rate, cardiac index, and pulse pressure and lower total peripheral resistance (all p less than 0.01) than men with the same pressure level. Isometric stress caused an increase in arterial pressure that was almost 50% higher in men than in women. The sexual difference in cardiovascular findings was significant before but not after menopause. For any level of arterial pressure, total peripheral resistance (and therefore the risk of hypertensive cardiovascular disease) was lower in women than in men. We conclude that premenopausal women are hemodynamically younger than men of the same chronologic age. Our study identifies a pathophysiologic mechanism for the clinical and epidemiologic finding that essential hypertension is less lethal in women than in men.

Adult↗