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Biomedical subjects

J Nappi

Publications and source records attributed to J Nappi.

9 recordsLinked to original sources
PubMed2000

Diastolic Heart Failure.

The diagnosis of diastolic heart failure (DHF) can be made when a patient has both symptoms and signs on physical exam of congestive heart failure (CHF), and normal left ventricular volume and ejection fraction. Documentation of abnormal diastolic function is confirmatory but not mandatory. Diastolic heart failure is a frequent cause of CHF (prevalence is 35% to 50%) and has a significant effect on mortality (5-year mortality rate is 25% to 35%) and morbidity (1-year readmission rate is 50%). Treatment should be targeted at symptoms, causal clinical disease, and underlying basic mechanisms. Symptom-targeted therapy: decrease pulmonary venous pressure using diuretics and long-acting nitrates, maintain atrial contraction and atrial ventricular synchrony, reduce heart rate using beta-adrenergic blockers and calcium channel blockers; increase exercise tolerance by reducing exercise- induced increases in blood pressure and heart rate using angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, and calcium channel blockers. Disease-targeted therapy: prevent or treat myocardial ischemia, prevent or regress left ventricular hypertrophy. Mechanism-targeted therapy (future directions): modify neurohumoral activation using renin, angiotensin, and aldosterone system antagonists (ACE inhibitors, angiotensin II receptor blockade, aldosterone and renin antagonist); endothelin antagonists; nitric oxide agonists; and atrial natruretic peptide agonists; alter intracellular mechanisms; alter extracellular matrix structures.

Journal Article↗
PubMed2000

Myocardial infarction in women: a critical appraisal of gender differences in outcomes.

In every year since 1984, cardiovascular disease has claimed the lives of more women than men. Data from randomized trials indicate that gender contributes to increased mortality after myocardial infarction independent of other risk factors, but additional confounding variables cannot be discounted. Data from registry databases indicate that women are less likely to receive medically proven therapies for myocardial infarction. Women experience more vague symptoms, which may account for underuse of effective therapies. In addition, they may benefit less from thrombolytic therapy than men. Increased use of thrombolytic therapy has resulted in a continued decrease in cardiovascular deaths for men, but not for women. It is unclear if this disparity is a result of inequitable access to therapy or decreased efficacy of these agents in women.

Adrenergic beta-Antagonists↗
PubMed1999

The association of the combination of sumatriptan and methysergide in myocardial infarction in a premenopausal woman.

Acute myocardial infarction occurred in a 43 year-old premenopausal woman with controlled hypertension and no known coronary artery disease following the use of the antimigraine medications sumatriptan succinate injectable form and methysergide maleate. The use of sumatriptan is contraindicated within 24 hours of using ergotamine or ergotamine-type medications such as methysergide. This contraindication is based on the theoretical possibility of prolonged vasospasm with the combined use. Methysergide is primarily a serotonin type 2 (5-HT2) antagonist, although it does act as a partial agonist at 5-HT1 receptors. It is believed that a major component of coronary artery vasospasm is possibly due to 5-HT supersensitivity mediated by 5-HT1Dbeta receptor activation. Drugs that selectively stimulate the 5-HT(D) receptors, such as sumatriptan, are potentially hazardous in people with underlying coronary artery disease, and agents with additional agonistic properties at these receptors may potentiate this effect. Physicians should be warned to inquire about prior 24-hour medication use before prescribing antimigraine medication.

Adult↗
PubMed1985

The lack of effect of nifedipine on failing skin flaps.

The calcium channel blocker, nifedipine, was administered to 16 pigs in randomized blinded fashion in an unsuccessful attempt to salvage failing random pattern flaps. Despite the moderate dose of drug used, nifedipine caused significant hypotension that may have countered any beneficial effect on small vessel flow. Further studies are needed before nifedipine is abandoned as a potential agent for the pharmacologic manipulation of failing skin flaps.

Animals↗
PubMed1983

Advances in the hemodialysis management of phenobarbital overdose.

When a comatose man requiring ventilatory support for acute ingestion of phenobarbital was admitted to the University of Utah Hospital, he was managed by a multispecialty team, which included a nephrologist and a clinical pharmacologist. Since the patient could not be moved to the dialysis unit, a mobile dialysis machine was used. A negative-pressure adapter was used in conjunction with a batch-type dialysis machine to create a single-pass dialysate delivery system. Blood was delivered to the dialyzer and returned to the patient through bilateral femoral catheters that had been placed percutaneously. Pharmacokinetic studies were performed and compared to the disappearance of phenobarbital by conservative measures alone after the patient had awakened and dialysis was discontinued.

Adult↗
PubMedDate not supplied

Clinical efficacy of amiodarone.

OBJECTIVES: To review the clinical efficacy and role of amiodarone in the management of supraventricular and ventricular arrhythmias and its effects on mortality. METHODS: Review of relevant studies and reports. RESULTS: Amiodarone exerts significant effects on atrial tissue. In most studies it was completely or partly effective in preventing recurrences of atrial fibrillation or flutter in up to 80% of patients. Amiodarone may be superior to class Ia agents for maintaining normal sinus rhythm. Large randomized trials indicate that it is a potent suppressor of ventricular arrhythmia and reduces arrhythmic death after myocardial infarction. In patients with cardiomyopathy, it suppresses asymptomatic arrhythmias and increases left ventricular ejection fraction. Meta-analysis of relevant studies indicated that amiodarone reduces the risk of arrhythmic and sudden death by 29% in high-risk patients with recent myocardial infarction or congestive heart failure. This translates into an overall 13% reduction in total mortality. CONCLUSION: Because of its effectiveness against a broad range of arrhythmias, amiodarone is a valuable addition to the antiarrhythmic pharmacopeia.

Amiodarone↗