[Influence of digitalis on the behavior of systolic time intervals induced with isometric exercise in coronary disease patients. Note VIII].
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Biomedical subjects
Publications and source records attributed to B Trimarco.
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The antihypertensive efficacy and tolerability of a calcium antagonist drug, diltiazem (60 mg q.i.d. per os), was compared with that of metoprolol (100 mg b.i.d. pr os) in a crossover, double-blind randomized trial in 20 patients with mild or moderate essential hypertension. Blood pressure and heart rate were assessed at rest and during bicycle exercise before and after four-week periods of treatment. Both metoprolol and diltiazem reduced significantly systolic and diastolic blood pressure, while heart rate decreased only after metoprolol therapy. The reduction in blood pressure and the percentage of patients who responded favorably were similar with the two drugs. Furthermore, the overall levels of blood pressure during exercise were significantly reduced by both treatments, while only metoprolol was able to reduce the maximum increase in systolic blood pressure and heart rate induced by exercise. These results suggest that the use of diltiazem may be appropriate to the treatment of patients with mild or moderate essential hypertension.
The antihypertensive efficacy of a new agent, indenolol, was compared with that of the well-established antihypertensive drug, metoprolol, and its hemodynamic effects were investigated using echocardiography. Eighteen hypertensives completed a double-blind, crossover, randomized study using indenolol and metoprolol. Two four-week courses with indenolol or metoprolol were preceded and followed by a two-week placebo period; the total duration of the study was 14 weeks. Indenolol proved to be significantly more effective than metoprolol in decreasing blood pressure values at rest (P less than .05). Furthermore, three patients that failed with metoprolol were successfully treated with indenolol. Both drugs induced a significant decrease in cardiac output that was mediated mainly through a reduction in heart rate, because stroke volume, left ventricle circumferential fiber shortening velocity, and ejection fraction were not significantly reduced by either drug. However, after indenolol, a significant direct relationship was found between the basal values of both cardiac output (r = .809) and total peripheral resistance (r = .800), and the reduction of these parameters. On the contrary, after metoprolol only, the correlation between the basal value of cardiac output and its reduction was significant (r = .790).
BACKGROUND: We compared rest-redistribution thallium 201 and resting technetium 99m methoxyisobutyl isonitrile (MIBI) cardiac imaging in 29 men with angiographically proven coronary artery disease and regional ventricular dysfunction. Left ventricular ejection fraction at radionuclide angiography was 35% +/- 9%. METHODS AND RESULTS: Regional left ventricular wall motion was assessed on gated 99mTc MIBI images according to a 3-point scale (0 = normal, 1 = hypokinetic, 2 = akinetic or dyskinetic). 201Tl and 99mTc MIBI uptake values were analyzed quantitatively. A total of 435 myocardial segments were classified on the basis of wall motion analysis into three groups: group 1 (normal wall motion; n = 201), group 2 (hypokinetic; n = 132), and group 3 (akinetic or dyskinetic; n = 102). 201Tl and 99mTc MIBI uptake values were significantly higher in groups 1 and 2 compared with group 3 (p < 0.05) and in group 1 compared with group 2 (p < 0.05). When 201Tl and 99mTc MIBI uptake values were directly compared, no significant differences in group 1 and 2 were observed. In group 3, 99mTc MIBI uptake (67% +/- 14%) was significantly lower (p < 0.001) than initial (72% +/- 11%) and delayed 201Tl uptake (73% +/- 12%). CONCLUSION: Thus rest-redistribution 201Tl and resting 99mTc MIBI cardiac imaging reflect the severity of left ventricular dysfunction in coronary artery disease. However, in segments with severely impaired regional ventricular function, 201Tl uptake is significantly higher than 99mTc MIBI uptake.
The role of the sympathetic nervous system in the settings of cardiac hypertrophy is postulated on the basis of experimental and clinical evidence. Only recently, the intimate mechanisms underlying hypertrophic responses of cardiac cell have been explored. Recent evidence spots the role of adrenergic receptors in the activation of several intracellular pathways of signaling that lead to nuclear responses of myocardiocyte. The molecular structures involved in these pathways may represent novel targets of future therapeutic interventions for cardiac hypertrophy and vascular remodeling in hypertension.
1. This study was designed to compare the response of plasma arginine vasopressin (AVP) to head-up tilt in hypertensive patients and in normals. 2. As expected, plasma AVP showed a consistent increase (P less than 0.005) in normal subjects after tilt while plasma volume decreased significantly (P less than 0.02). On the contrary, in hypertensive patients, after tilt both plasma AVP (P less than 0.025) and plasma volume (P less than 0.05) decreased. 3. These findings, thus, indicate that essential hypertension is characterized by an inverted response of arginine vasopressin to postural change.
We investigated the upright bicycle exercise cardiopulmonary response in 20 patients with left ventricular dysfunction (LVD, secondary to previous myocardial infarction, left ventricular ejection fraction range 18-44%). Ten patients (48 +/- 7 years) asymptomatic (I NYHA class) without drug treatment (LVD group). The others (n = 10) (50 +/- 1 years) complained of dyspnea and/or fatigue despite therapy (NYHA II-III). They represented the heart failure (HF) group. Eight sedentary men (40 +/- 10 years) served as controls. Controls and patients performed stress testings under drug treatment, when administered. Anaerobic ventilatory threshold (ATge) was considered as an index of submaximal exercise while peak exercise VO2 (Peak VO2) was considered the maximal volitional exercise capacity. The ratio between minute ventilation (VE) to carbon dioxide release (VCO2) (VE/VCO2) was assessed to evaluate the ventilatory response during exercise. We coupled gas exchange assessment (2001, MGC) with noninvasive monitoring of stroke volume (SV) by impedance cardiography (NCCOM3, BOMED) and total systemic vascular resistances (TSVR; by auscultatory blood pressure measurement). In controls VO2 increase during exercise was related to higher heart rate (HR) and SV both from resting to ATge and from this point to the peak. TSVR declined during both steps. In patients with HF VO2 rose from resting to ATge (by faster HR and unchanged SV). VO2 increased slightly from this point to Peak VO2. This result was related to flat HR increase and unchanged SV as well as TSVR. In patients with LVD VO2 increased similarly to controls from resting to ATge and less above the threshold. In these patients both HR and SV increased during submaximal exercise. From ATge to Peak VO2 only HR increased. TSVR declined significantly similarly to controls. The VE/VCO2 ratio was higher at peak exercise in patients with HF compared to controls. Different determinants were demonstrated in patients with left ventricular dysfunction with mild or symptomatic chronic heart failure (CHF). These findings and the increased ventilatory response in patients with CHF can explain different changes of VO2 in these patients during submaximal and maximal voluntary exercise and contribute to explain exercise-induced exertion in these subjects.
To investigate the impairment of beta-adrenoceptor responsiveness in human hypertension, we evaluated the effect of an oral salt load (400 mEq/day of NaCl for 7 days) on plasma catecholamine concentrations and beta-adrenoceptor-mediated effects in 11 young patients with mild essential hypertension. Responses of heart rate and plasma cAMP to isoproterenol administration were used as indices of beta-adrenoceptor responsiveness. Salt loading induced a significant reduction in the dose of isoproterenol required to raise the heart rate by 25 bpm (CD25) (from 7.6 +/- 1.5 to 5.3 +/- 0.9 micrograms, p less than 0.05) and an increase in the slopes of the regression lines for heart rate changes and isoproterenol doses (delta HR/IS) (from 3.3 +/- 0.6 to 4.7 +/- 0.7, p less than 0.05) and for plasma cyclic AMP (cAMP) level changes and isoproterenol doses (delta cAMP/IS) (from 0.3 +/- 0.06 to 1.4 +/- 0.3, p less than 0.05). After salt loading there was a significant reduction in plasma catecholamine concentrations with a significant relationship between changes in upright plasma epinephrine levels and changes in CD25 (r = 0.904, p less than 0.01) and in the slopes for delta HR/IS (r = 0.983, p less than 0.001) and delta cAMP/IS (r = 0.922, p less than 0.001). These results support the hypothesis that the impairment of beta-adrenoceptor sensitivity observed in human hypertension is associated with a beta-adrenoceptor overstimulation due to chronically elevated adrenergic tone.
Echocardiographic studies have shown a decrease in left ventricular (LV) wall thickness and an improvement in LV function during antihypertensive treatment. A reduction in LV mass parallels the reduction in LV wall thickness during the first year of antihypertensive treatment, but thereafter favorable changes in LV wall thickness, cardiac output, and total peripheral resistance may be recorded in spite of a constant LV mass. The reason for this is that LV mass is defined by LV wall thickness and LV end-diastolic diameter, and that LV mass may stay unchanged if LV wall thickness decreases when LV diameter increases. This pattern of change is to be expected since LV distensibility and, hence, LV end-diastolic diameter may increase when LV wall thickness decreases. The effect of treatment may thus be divided into two main phases--an initial phase with a reduction in LV mass and a reduction in cardiac output and no change in total peripheral resistance--and a second phase with a constant LV mass but an increase in cardiac output to the pretreatment level again and a concomitant decrease in total peripheral resistance. The increase in stroke volume and cardiac output during this second phase of treatment is mainly dependent on an increase in end-diastolic volume, most likely explained by improved LV compliance when LV wall thickness decreases. The concomitant decrease in total peripheral resistance is mainly explained by reversal of structural vascular changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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One hundred patients with primary hypercholesterolemia (total plasma cholesterol greater than or equal to 6.2 mmol/L [240 mg/dl]) were enrolled in an open, randomized, parallel comparative study of simvastatin and pravastatin. All patients started or continued a standard lipid-lowering diet for at least six weeks prior to entry into the four-week placebo baseline period. Fifty patients received simvastatin and 50 patients received pravastatin, both at the recommended starting dose of 10 mg/day, for a treatment period of six weeks. Total cholesterol levels were reduced by 24% (from 7.59 mmol/L to 5.80 mmol/L) with simvastatin, and by 15% (from 7.48 mmol/L to 6.35 mmol/L) with pravastatin. Low-density-lipoprotein cholesterol levels were reduced by 33% and 22% and high-density-lipoprotein cholesterol levels were increased by 10% and 7% with simvastatin and pravastatin, respectively. Plasma total triglyceride levels were reduced by 12% with simvastatin and by 6% with pravastatin. Adverse experiences were similar between treatment groups and both drugs were well tolerated. No patients were withdrawn from the study due to clinical adverse experiences; one patient in the pravastatin group required a reduction in dose to 5 mg/day due to insomnia. At the recommended starting dose, simvastatin had a significantly greater lipid-lowering effect than pravastatin. These results may have implications for the appropriate lipid-reduction therapy for patients at risk of coronary heart disease.