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Biomedical subjects

W H Frishman

Publications and source records attributed to W H Frishman.

At least 19 recordsLinked to original sources
PubMed2006

Pathophysiology and medical management of systemic hypertension and pre-eclampsia in pregnancy.

Hypertension in pregnancy includes a group of distinct disorders that require special consideration in both prevention and pharmacological treatment. In recent years, there have been few advances regarding the pathophysiology and prevention of pre-eclampsia, however there have been some promising studies regarding possible modes of screening women for preeclampsia before clinical signs and symptoms are apparent. The recommendations for first-line drug therapy for the hypertensive complications of pre-eclampsia, and the recommendations for pharmacological treatment of women with chronic hypertension antedating pregnancy, have changed little primarily because first-line medications have the advantage of having had more extensive research experience. Recent clinical trials have demonstrated the efficacy and safety of various second-line drugs for the hypertensive disorders of pregnancy; whether these therapies can eventually replace the standard recommended medications will require more extensive long-term investigation.

Adult↗
PubMed2001

One-year study of felodipine or placebo for stage 1 isolated systolic hypertension.

Asubstantial number of older hypertensive patients have stage 1 isolated systolic hypertension (systolic blood pressure between 140 and 159 mm Hg and diastolic blood pressure <90 mm Hg), but there are currently no data showing that drug treatment is effective, safe, and/or beneficial. To compare the effects of active treatment compared with placebo on blood pressure, left ventricular hypertrophy, and quality of life among older stage 1 isolated systolic hypertensive patients, a randomized, double-blind, parallel-group, multicenter clinical trial comparing felodipine (2.5, 5, or 10 mg once daily) and matching placebo was performed in 171 patients (49% male, average age 66+/-7 years, with 49% white and 30% Hispanic) with a baseline blood pressure of 149+/-7/83+/-6 mm Hg. During 52 weeks of treatment, patients randomized to active treatment achieved significantly lower blood pressures (137.0+/-11.7/80.2+/-7.6 mm Hg for extended-release felodipine versus 147.5+/-16.0/83.5+/-9.7 mm Hg for placebo, P<0.01 for each), a reduced incidence of left ventricular hypertrophy (7% for extended release felodipine versus 24% for placebo, P<0.04), and improved quality of life (change in Psychological General Well-Being index, 3.0+/-6.8 for extended-release felodipine versus -0.8+/-10.3 for placebo, P<0.01) versus baseline. There were no clinically significant differences between treatments in tolerability or adverse effects. Stage 1 isolated systolic hypertension can be effectively and safely treated pharmacologically. Treatment reduced progression to the higher stages of hypertension, reduced the incidence of left ventricular hypertrophy, and improved an overall measure of the quality of life. Larger and longer studies will be needed to document any long-term reduction in cardiovascular event rates associated with treating stage 1 systolic hypertension.

Aged↗
PubMed2000

Drug therapy of heart failure caused by systolic dysfunction in the elderly.

The presence of multiple medical illnesses often distinguishes elderly patients with heart failure and can make pharmacologic management of symptomatic heart failure challenging in this population. Physiologic changes that occur with normal aging may complicate clinical assessment. Limited data from large clinical trials of heart failure therapy are applicable to aged patients. Available data suggest that elderly patients should be treated with the same regimen as younger patients but that more careful attention should be paid to dosing, especially when initiating a new drug. History and physical examination techniques can be used to uncover evidence of congestion and inadequate perfusion and are critical adjuncts when making therapeutic decisions. The objectives of therapy for elderly patients with heart failure must be individualized within the larger context of patients' goals and stage of life.

Adrenergic Antagonists↗
PubMed2000

Cardiovascular drug therapy in patients with hepatic diseases and patients with congestive heart failure.

Hepatic impairment can alter the pharmacokinetic profiles of cardiovascular drugs, which can lead to unwanted toxicity. In the presence of cirrhosis, portosystemic shunting occurs and cytochrome P450 activity is reduced. Impaired oxygen uptake caused by changes in the liver's sinusoids, as proposed by the oxygen limitation theory, may also explain the alteration of drug metabolism seen in cirrhosis. With congestive heart failure, sinusoidal congestion and hypoperfusion of the liver are seen. Similar to cirrhosis, the common pathway for hepatic damage in congestive heart failure seems to be liver hypoxia, which may explain the disease's effect on drug metabolism. Since routine hepatic function tests do not always relate to the liver's ability to eliminate drugs, existing guidelines for dosing cardiovascular drugs in patients with hepatic impairment are limited. This article provides guidance for dosing cardiovascular drugs in cirrhotic and heart failure patients based on available research data. Altered drug metabolism, especially in congestive heart failure, tends to be overlooked or not realized in clinical practice. Therefore, further research is needed in congestive heart failure to better elucidate safe prescribing patterns.

Cardiovascular Agents↗
PubMed2000

Serotonin and the heart.

Serotonin is a naturally occurring vasoactive substance that has diverse cardiophysiological effects. These effects can be explained by the existence of serotonin receptor subtypes which mediate different biological actions. The vasoconstrictive actions of serotonin are mediated by 5-HT2 serotonergic receptors, and serotonin also amplifies the release and activities of other vasoconstrictors, such as angiotensin and norepinephrine. Abnormalities in the serotonergic system may play an important role in the pathophysiology of multiple cardiovascular disease states such as systemic hypertension, primary pulmonary hypertension and peripheral vascular disease. Selective 5-HT2 serotonergic receptor blockers have been developed which appear to be potent vasodilators with therapeutic potential in various cardiovascular disease states. The largest clinical experience has been collected with ketanserin, and other agents in this class are being investigated. Prolongation of the ECG QT interval with 5-HT2 serotonergic receptor blockers may pose a potential risk with these treatments in some patients.

Animals↗
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

Secondary prevention of myocardial infarction: role of beta-adrenergic blockers and angiotensin-converting enzyme inhibitors.

beta-Blockers reduce cardiovascular death and reinfarction in patients with a history of myocardial infarction (MI), and angiotensin-converting enzyme (ACE) inhibitors provide an overall survival benefit in patients with signs or symptoms of left ventricular (LV) dysfunction and a history of acute MI. Despite this, these agents remain underused in clinical practice. Appropriate patient selection in standard clinical practice should be encouraged in order to achieve a mortality rate reduction comparable to that seen in clinical trials. It appears from the findings of recent studies that the greatest benefit from beta-blocker therapy is achieved in patients who are more than 60 years of age and in patients at moderate or high risk for reinfarction and death (eg, patients with LV dysfunction or arrhythmias or both). Patients with class I-IV heart failure treated with ACE inhibitors have fewer recurrent infarctions, a lower incidence of severe congestive heart failure, and a reduced incidence of total cardiovascular death and sudden cardiac death. In addition to the studies completed in patients with MI, there are ongoing studies evaluating whether or not ACE inhibitors can reduce myocardial ischemic events in patients without a prior infarction who have coronary artery disease or hypertension and preserved LV function. There is also growing evidence that concomitant therapy with a beta-blocker and an ACE inhibitor may reduce mortality rates beyond that observed with ACE inhibitors alone in survivors of MI who have LV dysfunction.

Adrenergic beta-Antagonists↗
PubMed1999

Efficacy of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors for prevention of stroke.

OBJECTIVE: To determine if 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are effective in preventing fatal and nonfatal strokes in patients at increased risk of coronary artery disease. DESIGN: Meta-analysis of randomized controlled trials. Clinical trials were identified by a computerized search of MEDLINE (1983 to June 1996), by an assessment of the bibliographies of published studies, meta-analyses and reviews, and by contacting pharmaceutical companies that manufacture statins. Trials were included in the analysis if their patients were randomly allocated to a statin or placebo group, and reported data on stroke events. Thirteen of 28 clinical trials were selected for review. Data were extracted for details of study design, patient characteristics, interventions, duration of therapy, cholesterol measurements, and the number of fatal and nonfatal stroke events in each arm of therapy. Missing data on stroke events were obtained by contacting the investigators of the clinical trials. MAIN RESULTS: Among 19,921 randomized patients, the rate of total stroke in the placebo group was 2.38% (90% nonfatal and 10% fatal). In contrast, patients who received statins had a 1.67% stroke rate. Using an exact stratified analysis, the pooled odds ratio (OR) for total stroke was 0.70 (95% confidence interval [CI] 0.57, 0.86; p =.0005). The pooled OR for nonfatal stroke was 0.64 (95% CI 0.51, 0.79; p =.00001), and the pooled OR for fatal stroke was 1.25 (95% CI 0.71, 2.24; p =.4973). In separate analyses, reductions in total and nonfatal stroke risk were found to be significant only for trials of secondary coronary disease prevention. Regression analysis showed no statistical association between the magnitude of cholesterol reduction and the relative risk for any stroke outcome. CONCLUSIONS: The available evidence clearly shows that HMG-CoA reductase inhibitors reduce the morbidity associated with strokes in patients at increased risk of cardiac events. Data from 13 placebo-controlled trials suggest that on average one stroke is prevented for every 143 patients treated with statins over a 4-year period.

Aged↗
PubMed1999

Comparison of telmisartan with lisinopril in patients with mild-to-moderate hypertension.

In this study, telmisartan, a new angiotensin AT ( 1 ) receptor antagonist given as monotherapy and in combination with hydrochlorothiazide (HCTZ), was compared with lisinopril as monotherapy and in combination with HCTZ. This 52-week, randomized, multicenter, double-blind, double-dummy, parallel-group, dose-titration study of 578 patients with mild-to-moderate essential hypertension (mean diastolic blood pressure [DBP], >/=95 mm Hg), compared the efficacy and safety of telmisartan (n = 385) with lisinopril (n = 193). Dosage could be increased for both telmisartan (40 --> 80 --> 160 mg) and lisinopril (10 --> 20 --> 40 mg) at each of the first 2 monthly visits if DBP control (<90 mm Hg) had not been established. Once DBP control was established, patients entered the 48-week maintenance period. During this period, the dose of the study drug was fixed, although open-label HCTZ at 12.5 mg or 25 mg was added, when needed, to regain DBP control. At the end of the titration period, DBP control was achieved on monotherapy by 67% and 63% of the telmisartan and lisinopril patients, respectively. At the end of the maintenance period, supine DBP was controlled in 83% and 87% of the telmisartan and lisinopril patients, respectively, with systolic blood pressure over DBP reductions of 23.8/16.6 mm Hg for telmisartan and 19.9/15.6 mm Hg for lisinopril. Treatment-related side effects occurred in fewer telmisartan-treated patients (28%) than in lisinopril-treated patients (40%; P =.001). Significantly fewer patients (P =.018) receiving telmisartan experienced treatment-related cough (3% v 7%), and cough led to discontinuation significantly less often (P =.007) with telmisartan treatment than with lisinopril treatment (0.3% v 3.1%). In addition, two cases of angioedema were observed, both in the lisinopril group. The selective AT (1) receptor antagonist, telmisartan, is extremely effective in the treatment of mild-to-moderate hypertension both as monotherapy and in combination with HCTZ and is at least comparable in efficacy to lisinopril, with a tolerability profile that may offer advantages in terms of a reduced incidence of adverse events.

Angioedema↗
PubMed1999

Testosterone and other anabolic steroids as cardiovascular drugs.

There has been much interest in the effect of sex hormones on cardiovascular risk factors and as a therapeutic modality in both men and women. In this article, testosterone is considered as a possible therapy for cardiovascular disease. It has been shown that the level of serum testosterone decreases in men as they age. Healthy men with low testosterone levels have increased cardiovascular risk factors, including high fasting and 2-hour plasma glucose, serum triglycerides, total cholesterol and low-density lipoprotein (LDL) cholesterol, and apo A-I lipoprotein. Injections of testosterone to raise the levels to midnormal range have been shown to decrease total cholesterol and LDL cholesterol, while increasing high-density lipoprotein (HDL) cholesterol. Testosterone affects the clotting system by increasing thromboxane A (2) receptor activity and platelet aggregability. Testosterone has also been shown to augment the fibrinolytic system and antithrombin III activity. In men, testosterone has been shown to have antianginal effects, and endogenous levels have an inverse relationship to systolic blood pressure. Testosterone can be given in oral, injectable, pellet, and transdermal patch forms. There may be a role in administering testosterone to return men to normal physiologic range who have low serum levels. This treatment increases the risk of prostatic cancer, benign prostatism, erythrocytosis, and edema. No long-term studies of the effects of long-term testosterone replacement have been undertaken, so it is difficult to recommend this treatment as yet, but it is being considered as a therapy for augmenting skeletal muscle strength in patients with congestive heart failure.

Anabolic Agents↗
PubMed1999

Alpha-adrenergic blocking drugs in clinical medicine.

The alpha-adrenergic blockers have played an important role in the treatment of vascular diseases. Nonselective alpha blockers have been used as treatments for patients with severe hypertension, including pheochromocytoma. Selective alpha 1 blockers have been used in the treatment of hypertension and prostatic obstruction, and these drugs have also been considered in the treatment of other vascular and nonvascular conditions. They have unique metabolic actions, specifically on plasma lipids and lipoproteins, which could be of clinical benefit.

Adrenergic alpha-Antagonists↗
PubMed1999

Raloxifene, a new selective estrogen receptor modulator.

There is evidence from observational studies that estrogen replacement therapy in postmenopausal women can reduce the rates of morbidity and mortality of atherosclerotic heart disease. The mechanism of this cardiovascular protective effect is not yet established, but favorable actions of hormone therapy on plasma lipids and vascular endothelial function have been proposed. Estrogens can also increase the risk of breast and uterine carcinoma. The new selective estrogen receptor modulator (SERM) raloxifene appears to have benefits similar to estrogen on plasma lipids and osteoporosis, but it does not affect the rate of uterine carcinoma as does tamoxifen and estrogen. Animal studies suggest an anti-atherosclerotic action of raloxifene, but this needs to be confirmed in long-term human studies.

Animals↗
PubMed1999

Antiplatelet therapy: glycoprotein IIb/IIIa receptor antagonists.

The glycoprotein IIb/IIIa antagonists are potent drugs that inhibit platelet aggregation. They are formulated as monoclonal antibodies and synthetic peptides for intravenous use in patients undergoing high-risk angioplasty procedures and in patients with unstable coronary syndromes. Orally active agents are now being evaluated in clinical trials.

Journal Article↗
PubMed1999

How to use calcium antagonists in hypertension: putting the JNC-VI guidelines into practice. Joint National Committee for the Prevention, Detection, Evaluation and Treatment of High Blood Pressure.

The prevention and treatment of hypertension remain as major challenges for clinicians all over the world. The recently published Sixth Report of the Joint National Committee for the Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC-VI) uses evidence-based medicine in providing guidelines to aid clinicians in the prevention, detection and treatment of high blood pressure, including pharmacological approaches. Calcium antagonists are used widely for the treatment of hypertension, and JNC-VI focuses on specific situations where calcium antagonists could be considered as preferred treatments. There are a large number of calcium antagonists available, with a variety of pharmacodynamic and pharmacokinetic actions. Several sustained-release formulations of these drugs are also available. In terms of blood pressure control, calcium antagonists are more effective as antihypertensive treatments than beta-blockers, ACE inhibitors and angiotensin II receptor blockers in Black patients. The dihydropyridine calcium antagonists have been shown to reduce morbidity and mortality in elderly patients with isolated systolic hypertension. The rate-lowering calcium antagonists can be used as alternatives to beta-blockers in patients with coronary artery disease and hypertension. Calcium antagonists can be used as alternatives to ACE inhibitors in patients with hypertension and concomitant diabetes mellitus and/or renal disease. Some dihydropyridine calcium antagonists may be useful as alternatives to ACE inhibitors in patients with hypertension and systolic heart failure. Calcium antagonists appear to be extremely useful in patients with cyclosporin-induced hypertension, and in patients with hypertension and concomitant Raynaud's phenomenon and/or migraine. The rate-lowering agents can be used in patients with atrial tachyarrhythmias and hypertension. Clinicians should be aware of drug-drug interactions involving calcium antagonists, especially after the recent problems with mibefradil. Although retrospective studies have caused controversy regarding the safety of calcium antagonists in patients with hypertension, recent prospective studies have revealed no major safety concerns with these drugs.

Age Factors↗
PubMed1998

Carvedilol.

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Adrenergic alpha-Antagonists↗