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Biomedical subjects

P C Deedwania

Publications and source records attributed to P C Deedwania.

At least 37 records · Page 2Linked to original sources
PubMed1999

Comparison of controlled-onset, extended-release verapamil with amlodipine and amlodipine plus atenolol on exercise performance and ambulatory ischemia in patients with chronic stable angina pectoris.

This multicenter, randomized, double-blind, parallel group, placebo lead-in, placebo-controlled study compared the antianginal and anti-ischemic effects of once-daily bedtime dosing of controlled-onset extended-release (COER-24) verapamil to a once-daily morning dosing of amlodipine +/- atenolol in patients with chronic stable angina. A total of 551 patients with exercise-induced myocardial ischemia and evidence of coronary artery disease were randomized to a 4-week, forced-dose titration treatment period with (1) COER-24 verapamil 240 mg titrated to 480 mg at bedtime (n = 173), (2) amlodipine 5 mg titrated to 10 mg/day (n = 149), (3) amlodipine 5 mg (titrated to 10 mg) plus atenolol 50 mg/day in the A.M. (n = 154), or (4) placebo (n = 75). Treadmill exercise tolerance testing (standard Bruce protocol), and 48-hour ambulatory electrocardiographic (Holter) monitoring were performed at the end of placebo lead-in and double-blind treatment. Each active treatment significantly improved symptom-limited exercise duration and time to moderate angina (p < or = 0.01 vs placebo). For patients with baseline ischemia, amlodipine resulted in a statistically significant increase in total duration of ischemic episodes compared with placebo, whereas COER-24 verapamil and amlodipine plus atenolol resulted in statistically significant decreases compared with placebo and amlodipine. Heart rate at onset of ischemic episodes and ST product were also significantly increased with amlodipine (p < 0.05) compared with either COER-24 or amlodipine plus atenolol. COER-24 and amlodipine alone or in combination with atenolol improved exercise capacity in patients with angina pectoris. COER-24 verapamil monotherapy or amlodipine plus atenolol combination therapy were more effective than amlodipine monotherapy in decreasing ambulatory myocardial ischemia, especially during the hours of 6 A.M. to 12 noon.

Adrenergic beta-Antagonists↗
PubMed1999

Effects of L-arginine on atherogenesis and endothelial dysfunction due to secondhand smoke.

Secondhand smoke (SHS) and hypercholesterolemia increase cardiovascular risk. We hypothesized that L-arginine, the precursor of nitric oxide (NO), might protect against atherogenesis and endothelial dysfunction caused by SHS. The effects of L-arginine supplementation (2.25% solution ad libitum) and SHS (smoking chambers for 10 weeks) were examined in 32 hypercholesterolemic rabbits. Eight normal rabbits served as controls. Acetylcholine- and nitroglycerin-induced vasorelaxation was assessed in aortic rings precontracted with norepinephrine. Hypercholesterolemia increased intimal lesion area (P=0.012), reduced endothelium-dependent relaxation (P=0.009), and reduced basal (P=0.005) and stimulated (P<0.0005) production of NOs. SHS increased intimal lesion area (P=0. 01) norepinephrine-induced contraction (P=0.001) and reduced endothelium-dependent relaxation (P=0.02). SHS-induced increase in norepinephrine contraction was abolished by the inhibition of NO synthase and removal of endothelium. L-Arginine improved endothelium-dependent relaxation (P=0.001) and attenuated SHS-induced endothelial dysfunction (P=0.007) and atherogenesis (P=0. 001). Basal production of nitrogen oxides correlated inversely with intimal lesion area (r=-0.66; P<0.0005) and stimulated production of NOs correlated with endothelium-dependent relaxation (r=-0.66; P<0. 001). SHS causes endothelial dysfunction and increased adrenergic responsiveness and atherogenesis in hypercholesterolemic rabbits. Chronic dietary supplementation with the NO precursor L-arginine mitigates these effects. The adverse vascular consequences of SHS appear to be mediated via deleterious effects on endothelial function.

Animals↗
PubMed1998

Spontaneous conversion and maintenance of sinus rhythm by amiodarone in patients with heart failure and atrial fibrillation: observations from the veterans affairs congestive heart failure survival trial of antiarrhythmic therapy (CHF-STAT). The Department of Veterans Affairs CHF-STAT Investigators.

BACKGROUND: In a multicenter, double-blind, placebo-controlled study, the long-term effects of amiodarone on morbidity and mortality in patients with congestive heart failure (CHF) and atrial fibrillation (AF) were evaluated during a 4-year period. METHODS AND RESULTS: Of 667 patients with CHF, 103 (15%) had AF at baseline. Of these, 51 were randomized to amiodarone and 52 to placebo. The group with sinus rhythm and the group in AF were comparable except for a higher proportion of AF in patients with nonischemic versus ischemic cardiomyopathy (41% versus 27%, P<0.005). The mean ventricular response (VR) during AF over 24 hours was reduced by amiodarone at 2 weeks (20%, P=0.001), at 6 months (18%, P=0.001), and at 12 months (16%, P=0.006). Maximal VR was reduced 22% (P=0.001) at 2 weeks, 19% (P=0.001) at 6 months, and 14% (P=0.001) at 12 months. Sixteen of 51 patients on amiodarone and 4 of 52 on placebo converted to sinus rhythm during the study (chi2=9.23, P=0.002). During follow-up, 11 of 268 patients in sinus rhythm on amiodarone at baseline and 22 of the 263 in sinus rhythm on placebo developed AF; the difference was significant (chi2=12.88, P=0.005). Analysis of total mortality during follow-up showed a significantly lower mortality rate (P=0. 04) in patients in AF at baseline who subsequently converted to sinus rhythm on amiodarone than in those who did not convert to sinus rhythm on the drug. CONCLUSIONS: In patients with CHF, amiodarone has a significant potential to spontaneously convert patients in AF to sinus rhythm, with patients who convert having a lower mortality rate than those who do not. The drug prevented the development of new-onset AF and significantly reduced the VR in those with persistent AF.

Aged↗
PubMed1998

A perspective on hyperlipidemia: concepts of management in the prevention of coronary artery disease.

The clinical benefits of lowering elevated serum cholesterol for both primary and secondary prevention of coronary artery disease are now well established. Reduction in clinical events occurs early and appears to be related to stabilization of atherosclerotic plaque. Despite these salutary findings, lipid-lowering therapy, both nondrug and pharmacologic, is still markedly underutilized in patients and high-risk individuals in the asymptomatic population. Recent practical and uncomplicated guidelines present a rational strategy for selection of patients for low-density lipoprotein (LDL) cholesterol reduction and have the potential to yield major clinical benefits if properly implemented. Preventive cardiology measures should be applied by matching the intensity of the intervention to the hazard for clinical events. We support the current guidelines of the expert panels described in this article and propose several extensions for cholesterol lowering in selected, high-risk populations.

Anticholesteremic Agents↗
PubMed1998

Outcomes in patients with acute non-Q-wave myocardial infarction randomly assigned to an invasive as compared with a conservative management strategy. Veterans Affairs Non-Q-Wave Infarction Strategies in Hospital (VANQWISH) Trial Investigators.

BACKGROUND: Non-Q-wave myocardial infarction is usually managed according to an "invasive" strategy (i.e., one of routine coronary angiography followed by myocardial revascularization). METHODS: We randomly assigned 920 patients to either "invasive" management (462 patients) or "conservative" management, defined as medical therapy and noninvasive testing, with subsequent invasive management if indicated by the development of spontaneous or inducible ischemia (458 patients), within 72 hours of the onset of a non-Q-wave infarction. Death or nonfatal infarction made up the combined primary end point. RESULTS: During an average follow-up of 23 months, 152 events (80 deaths and 72 nonfatal infarctions) occurred in 138 patients who had been randomly assigned to the invasive strategy, and 139 events (59 deaths and 80 nonfatal infarctions) in 123 patients assigned to the conservative strategy (P=0.35). Patients assigned to the invasive strategy had worse clinical outcomes during the first year of follow-up. The number of patients with one of the components of the primary end point (death or nonfatal myocardial infarction) and the number who died were significantly higher in the invasive-strategy group at hospital discharge (36 vs. 15 patients, P=0.004, for the primary end point; 21 vs. 6, P=0.007, for death), at one month (48 vs. 26, P=0.012; 23 vs. 9, P=0.021), and at one year (111 vs. 85, P=0.05; 58 vs. 36, P= 0.025). Overall mortality during follow-up did not differ significantly between patients assigned to the conservative-strategy group and those assigned to the invasive-strategy group (hazard ratio, 0.72; 95 percent confidence interval, 0.51 to 1.01). CONCLUSIONS: Most patients with non-Q-wave myocardial infarction do not benefit from routine, early invasive management consisting of coronary angiography and revascularization. A conservative, ischemia-guided initial approach is both safe and effective.

Angioplasty, Balloon, Coronary↗
PubMed1998

Tophaceous pseudogout of the mitral valve.

This report describes a 61-year-old patient on chronic hemodialysis with multiple, left-sided, intracardiac masses causing intermittent coronary obstruction. Mitral valve replacement was performed. Massive deposition of calcium pyrophosphate crystals in and around the valve cusps led to the diagnosis of tophaceous pseudogout (tumoral calcinosis) of the mitral valve.

Calcinosis↗
PubMed1998

Design and baseline characteristics of the Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital (VANQWISH) trial. VANQWISH Trial Research Investigators.

OBJECTIVES: The Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital (VANQWISH) trial was designed to compare outcomes of patients with a non-Q wave myocardial infarction (NQMI) who were randomized prospectively to an early "invasive" strategy versus an early "conservative" strategy. The primary objective was to compare early and late outcomes between the two strategies using a combined trial end point (all-cause mortality or nonfatal infarction) during at least 1 year of follow-up. BACKGROUND: Because of the widely held view that survivors of NQMI are at high risk for subsequent cardiac events, management of these patients has become more aggressive during the last decade. There is a paucity of data from controlled trials to support such an approach, however. METHODS: Appropriate patients with a new NQMI were randomized to an early "invasive" strategy (routine coronary angiography followed by myocardial revascularization, if feasible) versus an early "conservative" strategy (noninvasive, predischarge stress testing with planar thallium scintigraphy and radionuclide ventriculography), where the use of coronary angiography and myocardial revascularization was guided by the development of ischemia (clinical course or results of noninvasive tests, or both). RESULTS: A total of 920 patients were randomized (mean follow-up 23 months, range 12 to 44). The mean patient age was 61 +/- 10 years; 97% were male; 38% had ST segment depression at study entry; 30% had an anterior NQMI; 54% were hypertensive; 26% had diabetes requiring insulin; 43% were current smokers; 43% had a previous acute myocardial infarction; and 45% had antecedent angina within 3 weeks of the index NQMI. CONCLUSIONS: Baseline characteristics were compatible with a moderate to high risk group of patients with an NQMI.

Angina Pectoris↗
PubMed1998

In-utero and neonatal exposure to secondhand smoke causes vascular dysfunction in newborn rats.

OBJECTIVES: We sought to determine the effects of secondhand smoke (SHS) exposure on vascular reactivity in newborn and infant rats. BACKGROUND: Secondhand smoke exposure increases cardiovascular risk. Secondhand smoke-induced endothelial dysfunction has been demonstrated in older teenagers and young adults. We have previously shown in adult rabbits that SHS induces atherogenesis and endothelial dysfunction. The effects of SHS on vascular function in the offspring of SHS-exposed mothers and in infants are unknown. METHODS: In this study the effects of in-utero (21 days) and neonatal (28 days) exposure to SHS were examined in 80 rats, 4 weeks of age, in a 2-by-2 design study. Rats were exposed to sidestream smoke in smoking chambers. Aortic rings were excised and isometric force responses to phenylephrine, acetylcholine, A23187 and nitroglycerin were studied in organ baths. RESULTS: Neonatal SHS exposure reduced animal weight (p=0.009). In-utero exposure increased the sensitivity (decreased the EC50) of aortic rings to phenylephrine (p < 0.0005), as did neonatal exposure (p=0.01). Maximal contraction to phenylephrine was reduced by in-utero exposure (p=0.04). In-utero SHS exposure reduced maximal endothelium-dependent relaxation to acetylcholine (p=0.04) and increased the EC50 (p=0.05), suggesting impaired sensitivity to acetylcholine. In-utero exposure decreased the sensitivity (increased the EC50) to the endothelium-independent vasodilator nitroglycerin (p=0.003). CONCLUSIONS: Secondhand smoke has detrimental effects on vascular smooth muscle function in the newborn.

Acetylcholine↗
PubMed1998

Antioxidant diet preserves endothelium-dependent vasodilatation in resistance arteries of hypercholesterolemic rabbits exposed to environmental tobacco smoke.

Environmental tobacco smoke (ETS) has been shown to impair endothelium-dependent vasodilation in vitro. This study was performed to investigate the effect of ETS on acetylcholine (ACh)-mediated blood pressure changes in vivo. Seventeen New Zealand White rabbits were fed a cholesterol diet (0.3%) for 13 weeks. Ten animals were exposed to ETS for 6 h/day, and seven animals were not exposed to ETS (non-ETS). Four of the ETS and three of the non-ETS-exposed rabbits received an antioxidant vitamin diet before and during their cholesterol diet for 21 weeks. Six rabbits served as healthy controls. To determine endothelium-dependent and independent blood pressure (BP) responses, BP was measured through a Tygon catheter, inserted into the right carotid artery at baseline and after each of three incremental intravenous doses of norepinephrine (NE; 1, 4, and 20 microg/kg), ACh (3.3, 10, and 30 microg/kg), and nitroglycerin (NTG; 1, 10, and 40 microg/kg). After NE, BP increases were significantly attenuated in the ETS group (p = 0.001) but not in animals receiving the antioxidant supplement. At both the middle and high ACh concentrations, ETS (p = 0.03 and p = 0.01, respectively) and hypercholesterolemia (p = 0.03 and p = 0.06, respectively) attenuated ACh-induced reductions in BP. At the highest ACh concentration, vitamins enhanced the reduction in BP (p = 0.002) and blocked the effect of ETS (p = 0.04). Neither ETS nor vitamins influenced NTG-induced decreases in BP. A combined antioxidant-vitamin diet can preserve endothelium-dependent vasodilatation in the hypercholesterolemic rabbit exposed to ETS.

Acetylcholine↗
PubMed1998

Effects of antioxidant vitamins C and E on atherosclerosis in lipid-fed rabbits.

BACKGROUND: Antioxidant vitamins are hypothesized to help prevent atherosclerosis by blocking lipoprotein oxidation. We investigated the effects of dietary vitamins C and E on atherosclerosis in rabbits. METHODS AND RESULTS: Forty New Zealand male rabbits were divided into 4 groups: 0.3% cholesterol diet with (LV) and without vitamin (LC), and 0.5% cholesterol diet with (HV) and without vitamins (HC). The treated groups consumed 137 +/- 8 mg/day vitamin C and 80 +/- 4 mg/day vitamin E for 10 weeks. Vitamin treatment did not significantly affect serum lipids. Alpha-tocopherol values were significantly higher in both serum (mg/dl) and omental fat (microg/g) among the treated rabbits (3.9 +/- 0.5 and 31.6 +/- 2.1 for LV, 1.7 +/- 0.2 and 12.1 +/- 1.9 for LC, 5.6 +/- 0.8 and 51.3 +/- 9.3 for HV and 1.9 +/- 0.3 and 8.2 +/- 0.4 for HC; p < 0.001). Vitamin treatment did not affect the percent of surface lesions in the aorta and pulmonary artery (23.8 +/- 5.2 and 20.1 +/- 3.3% for LV, 19.8 +/- 5.6 and 23.2 +/- 3.5% for LC, 28.1 +/- 6.5 and 51.1 +/- 4.2% for HV and 32.4 +/- 5.5 and 43.7 +/- 3.9% for HC, respectively; p = 0.981 and p = 0.562. CONCLUSIONS: Although significantly higher values of alpha-tocopherol were found in both serum and omental fat, antioxidant vitamins C and E did not demonstrate a significant protective effect on atherosclerosis in lipid-fed rabbits during the 10-week study period.

Animals↗
PubMed1997

Role of beta blockade in the treatment of myocardial ischemia.

A number of antianginal drugs and therapeutic strategies are now available for the treatment of patients with coronary artery disease (CAD) and myocardial ischemia. Of the available antianginal drugs, beta blockers appear to be most effective in suppressing myocardial ischemia. The superior anti-ischemic efficacy of beta blockers can be explained by their beneficial actions on hemodynamic parameters, vasomotion, and platelet function. Compared with other anti-ischemic drugs, beta blockers appear to be more efficacious in reducing the magnitude of myocardial ischemia during routine daily activities. In addition, the results of recent studies indicate that treatment with beta blockers not only suppresses myocardial ischemia, but also improves the clinical outcome in patients with CAD. These beneficial effects, along with the well-demonstrated cardioprotective effects of beta blockade in the postinfarction period, clearly suggest that this class of anti-ischemic drugs is an ideal therapeutic choice in most patients with CAD.

Adrenergic beta-Antagonists↗