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M Kukin

Publications and source records attributed to M Kukin.

10 recordsLinked to original sources

New advances in the pharmacological management of chronic heart failure.

The management of heart failure has evolved in parallel with advances in the understanding of the disease process. Inotropes and diuretics are used to combat pump failure and fluid overload. While no convincing data has emerged regarding the long-term safety of inotropes, new exciting data concerning the role of diuretics, especially aldactone, has led to a renewed interest in this class of drug therapy. Angiotensin converting enzyme inhibitors (ACE inhibitors) were noted to not only affect symptomatology but also decrease mortality by interfering with the renin-angiotensin-aldosterone system. Recent research has focused on more complete blockade of the renin-angiotensin system than that achieved with ACE inhibitors alone with the addition of direct angiotensin II receptor blockers. This new class of drugs may become not only a reasonable alternative to ACE inhibitors in patients intolerant of the drug but also a possible addition to ACE inhibitors in the battle to prevent progression of remodelling and disease. beta-blockers are the most exciting new class of drugs used to combat heart failure. They appear not only to combat the remodelling process that occurs in the progression of disease but also other pathological events such as apoptosis and cellular oxidation. New medical therapies currently being investigated include novel agents such as endothelin antagonists, natriuretic peptides, vasopressin antagonists and anticytokine agents--all part of a new era in drug management of heart failure that has evolved with continued advances in the understanding of chronic heart failure (CHF).

Adrenergic beta-Antagonists↗

Current issues regarding beta-adrenergic blockade in patients with congestive heart failure: patient selection, nonselective versus selective blockade, management of adverse effects, and indications for withdrawal of therapy.

Neurohormonal activation and chronic adrenergic overstimulation appear to play important roles in mediating the progressive pathophysiology of congestive heart failure (CHF), and the beneficial effects of beta-blockade in the management of chronic heart failure have been demonstrated by multiple clinical trials over the last decade. Nevertheless, the initiation and maintenance of beta-blocker therapy in CHF may initially precipitate a deterioration in clinical function, and numerous questions regarding the appropriate use of these agents in patients with heart failure remain. This report examines the practicalities of beta-adrenergic blockade in heart failure, focusing on patient selection, nonselective versus selective blockade, management of adverse effects, and indications for withdrawal of therapy.

Adrenergic beta-1 Receptor Antagonists↗

beta-Blockers in congestive heart failure.

Recent advances in the understanding of the basic mechanisms underlying congestive heart failure (CHF) have focused on the role of neurohormonal activation. Chronic adrenergic overstimulation is directly toxic to myocardial cells, impairs function, causes peripheral vasoconstriction and may induce programmed cell death via apoptosis. beta-Adrenergic blockade can interrupt this pathological process. Accumulating evidence now points to a clear role for beta-blocking agents in the management of heart failure, reducing both the morbidity and mortality associated with CHF. This report will review the recent clinical trials supporting the use of beta-blockers in CHF, briefly highlight some practical considerations in the use of these drugs in patients with CHF and discuss several areas of controversy in which further study is needed.

Journal Article↗

Carvedilol [Coreg].

Explore the source record for details and available documents.

Adrenergic beta-Antagonists↗

Effect of oral sotalol on systemic hemodynamics and programmed electrical stimulation in patients with ventricular arrhythmias and structural heart disease.

We explored the central hemodynamic responses to oral sotalol during dose titration in patients with ventricular arrhythmias who underwent programmed ventricular stimulation. Twelve patients were included in the study, 9 with a history of sustained ventricular tachyarrhythmias (6 postmyocardial infarction and 3 with cardiomyopathy) and 3 with a history of nonsustained ventricular tachycardia postmyocardial infarction. Left ventricular ejection fractions were < 45% in 10 patients, and < 35% in 5; the mean ejection fraction was 37% (range 20-51%). Sotalol prevented the induction of ventricular tachycardia in each of 3 patients with nonsustained ventricular tachycardia and in 6 of 9 with sustained ventricular tachycardia at baseline study. At peak action (2 hours) after sotalol loading (mean dose, 167 mg orally twice daily), the hemodynamic effects included bradycardia, decreased cardiac index, increased left ventricular filling pressure and systemic vascular resistance, and no change in stroke volume or stroke work index. One patient was not continued on sotalol, owing to an excessive increase in the pulmonary capillary wedge pressure, despite the lack of symptomatic heart failure. Congestive heart failure in association with marked bradycardia developed in another patient, who had suppression of inducible ventricular tachycardia after sotalol loading; this patient was managed with a reduction in the dose of sotalol and a regimen of digoxin and furosemide, and has been well compensated and without a recurrence of sustained ventricular tachycardia for more than 4 years. Ventricular tachycardia has been controlled with sotalol, without hemodynamic deterioration, in 6 of these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Relation between exercise-induced changes in ejection fraction and systolic loading conditions at rest in aortic regurgitation.

To examine the role of systolic wall stress at rest in determining left ventricular performance during exercise in aortic regurgitation (AR), systolic wall stress (measured by M-mode echocardiography) was related to changes in left ventricular function during maximal exercise (evaluated by radionuclide ventriculography) in 30 patients with chronic aortic regurgitation. Of these 30 patients, 7 had a normal exercise response, defined as an absolute increase in ejection fraction of 5% or greater (Group I) and 23 had abnormal exercise response, defined as no change (less than 5% change) or a decline (less than or equal to 5%) in ejection fraction (Group II). Patients in Group I had a significantly lower radius/wall thickness ratio (2.5 +/- 0.2 versus 3.1 +/- 0.1, p less than 0.01) and lower peak systolic wall stress (123 +/- 11 versus 211 +/- 12 X 10(3) dynes/cm2, p less than 0.01) than patients in Group II. An increase in ejection fraction during exercise was seen in 6 of the 9 patients with normal systolic wall stress at rest (less than 150 X 10(3) dynes/cm2), but in only 1 of 21 patients with elevated systolic wall stress (p less than 0.001). Peak systolic wall stress at rest varied linearly, and inversely with changes in left ventricular ejection fraction during exercise (r = 0.60, p less than 0.001). Groups I and II did not differ in ejection fraction at rest, clinical symptoms or maximal work load achieved.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Oxidative stress and congestive heart failure.

Oxygen free radicals, produced by the reduction of oxygen during many cellular reactions, have been implicated in the pathogenesis of a variety of cardiovascular diseases. Extremely reactive, free radicals damage many cellular structures and interfere with multiple cell functions. Clinically, free radicals have been associated with coronary atherosclerosis, ischemia, and reperfusion injury (“stunning”), and other processes related to chronic myocardial dysfunction. Several studies have reported elevated markers of free radical mediated injury in patients with congestive heart failure (CHF), and the link between oxidative stress and the genesis and progression of chronic CHF is being increasingly explored. This review briefly highlights free radical biology and examines the rationale and evidence for the role of oxidative stress in chronic heart failure. (c)1999 by CHF, Inc.

Journal Article↗