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Biomedical subjects

Andrew J Burger

Publications and source records attributed to Andrew J Burger.

27 records · Page 2Linked to original sources
PubMed2002

The effect of sex on ventricular arrhythmic events in patients with congestive heart failure.

The propensity to develop specific arrhythmias varies between the sexes. Patients with congestive heart failure (CHF) have a high prevalence of ventricular ectopy. However, it is not known if sex related differences exist in the susceptibility to arrhythmias in the setting of CHF. The study population included 159 men and 77 women (mean age 61 +/- 14 years) admitted for decompensated CHF. The severity of atrial and ventricular arrhythmias was assessed by 24-hour Holter monitoring. None of the patients were on parenteral vasoactive therapy during Holter recording. All measures of ventricular ectopy were markedly lower in women compared to men. The mean hourly ventricular pairs (283 +/- 67 vs 106 +/- 30, P = 0.04), mean hourly repetitive ventricular beats (28 +/- 7 vs 10 +/- 3, P = 0.04), and the frequency of ventricular tachycardia episodes per 24 hours (31 +/- 9 vs 7 +/- 3, P = 0.01) were significantly lower in women. After inclusion of clinical variables and drug therapies in a multivariate analysis, the negative relationship between female sex and the frequency of ventricular pairs (P = 0.04), repetitive ventricular beats (P = 0.04), and ventricular tachycardia episodes (P = 0.0005) remained independent. No differences in atrial ectopy between men and woman were found. Complex ventricular ectopy and episodes of ventricular tachycardia are significantly lower in women with CHF. Whether these finding are relevant to female survival advantage in the setting of heartfailure can only be determined by a prospective study. Further understanding of the mechanisms involved in the protection conferred by the patient's sex would advance our understanding about arrhythmias in heart failure.

Adult↗
PubMed2002

False positive ST segment elevation during dobutamine stress echocardiography due to left ventricular hypertrophy.

The significance of ST segment elevation in dobutamine stress echocardiography (DSE) remains controversial. In patients with prior Q wave myocardial infarction (MI), it may reflect myocardial ischemia, contractile reserve in the infarct-related area, or dyskinesia of the infarcted areas of myocardium. In the nonpost-MI population, it has been attributed to vasospasm or strongly associated with coronary artery disease and ischemia. We hypothesized that ST segment elevation in the absence of inducible ischemia or prior MI is related to the presence of left ventricular hypertrophy (LVH). During DSE, dobutamine was infused from 5 microg/kg/min up to a maximum of 50 microg/kg/min. Echocardiographic images were obtained at baseline, low dose, peak dose, and recovery. Ischemia was defined as either the development of a new wall-motion abnormality or worsening wall motion at peak dose. We reviewed 682 consecutive DSE tests and found ST elevation in 42 patients (incidence = 6.1%). After excluding two patients for > 10% uninterpretable echocardiographic segments, the study population consisted of 40 patients. In 25 patients with ST elevation and without echocardiographic evidence for dobutamine-induced ischemia, 21 (84%) patients had LVH (P = 0.001). In 15 patients with inducible ischemia, only 4 (27%) patients had LVH. No other significant differences were found except that prior MI was more common in the inducible ischemia group. In the subgroup of 18 patients without prior MI, no inducible ischemia was found in 15 (83%). LVH was present in 14 (93%) of these 15 patients (P < 0.005), and all 14 had a normal baseline left ventricular ejection fraction. None of the three patients in the nonpost-MI subgroup with inducible ischemia had LVH. The 22 patients with prior MI had no significant association with LVH (P = 0.39). We conclude that ST segment elevation during DSE can occur without echocardiographic evidence for ischemia and is associated with LVH in the nonpost-MI population. This ST elevation may be related to transient electrocardiographic repolarization changes in the hypertrophied ventricle in the presence of altered loading conditions and/or altered catecholamine influences rather than true ischemia.

Adrenergic beta-Agonists↗
PubMed2002

Concomitant beta-blocker therapy is associated with a lower occurrence of ventricular arrhythmias in patients with decompensated heart failure.

BACKGROUND: Ventricular arrhythmias are nearly universally present in patients with advanced congestive heart failure (CHF) and represent an important cause of mortality in these patients. One of the putative mechanisms for the salutary effects of beta-blockers on sudden death mortality in heart failure is their ability to suppress ventricular arrhythmias. However, supporting data in patients with CHF are sparse, especially in the setting of excessive neurohumoral activation associated with symptomatic decompensated heart failure. METHODS AND RESULTS: We studied 236 patients (159 men; mean age, 61 +/- 14 years) admitted for decompensated CHF. Fifty patients were receiving beta-blockers at the time of the study. The severity of ventricular arrhythmia was assessed by 24-hour Holter recordings by using several prospectively defined measures of ventricular ectopy. All measures of ventricular ectopy were lower in patients receiving beta-blockers. The average hourly total premature ventricular beats (PVCs), hourly ventricular couplets, repetitive PVCs, and frequency of ventricular tachycardia episodes were 15% (P =.02), 75% (P <.05), 72% (P <.05), and 87% (P =.01) lower in patient receiving beta-blockers, respectively. In a multivariate regression analysis, the negative relationship between beta-blockers and the average hourly PVCs (P =.03), the frequency of ventricular pairs (P =.03), repetitive PVCs (P <.05), and ventricular tachycardia episodes (P =.01) remained significant and independent. CONCLUSIONS: Concomitant beta-blocker therapy during heart failure decompensation is associated with a marked reduction in complex ventricular ectopy and episodes of ventricular tachycardia. This effect of beta-blockers may play an important protective role by preventing serious ventricular arrhythmias during transient increases in sympathetic activity.

Adrenergic beta-Antagonists↗
PubMed2002

Effect of nesiritide (B-type natriuretic peptide) and dobutamine on ventricular arrhythmias in the treatment of patients with acutely decompensated congestive heart failure: the PRECEDENT study.

BACKGROUND: Dobutamine is commonly used as a means of treating decompensated congestive heart failure (CHF). Although typically effective at improving short-term hemodynamics and symptomatology, the frequent occurrence of arrhythmias and tachycardia is undesirable. In this randomized, multicenter trial, we compared the safety and clinical effectiveness of the cardiac hormone nesiritide (human B-type natriuretic peptide) with dobutamine in hospitalized patients with decompensated CHF. METHODS: The study population consisted of 255 patients who were randomized to 1 of 2 doses of intravenous nesiritide (0.015 or 0.03 microg/kg/min) or dobutamine (> or =5 microg/kg/min) and stratified by means of an earlier history of ventricular tachycardia. Patients were also assessed with 24 hour Holter recordings immediately before and during study drug therapy and by means of signs and symptoms of CHF. RESULTS: Dobutamine significantly increased the mean (1) number of ventricular tachycardia events per 24 hours by 48 +/- 205 (P =.001), (2) repetitive ventricular beats per hour by 15 +/- 53 (P =.001), (3) premature ventricular beats per hour by 69 +/- 214 (P =.006), and (4) heart rate by 5.1 +/- 7.7 beats per minute (P <.001). These end points were significantly decreased or unchanged in the nesiritide groups. Nesiritide did not increase heart rate, despite a greater reduction of blood pressure. Both drugs were similarly effective means of improving signs and symptoms of CHF. CONCLUSIONS: Dobutamine is associated with substantial proarrhythmic and chronotropic effects in patients with decompensated CHF, whereas nesiritide actually reduces ventricular ectopy or has a neutral effect. Compared with dobutamine, nesiritide may be a safer, short-term treatment for patients with decompensated CHF.

Aged↗
PubMed2002

Age and sex as determinants of ventricular arrhythmic events in patients with decompensated congestive heart failure.

BACKGROUND: The propensity to develop specific arrhythmias varies between the sexes and is influenced by age. Patients with congestive heart failure (CHF) have a high prevalence of ventricular ectopy. However, in the setting of CHF, it is not known whether sex-related or age-dependent differences exist in the susceptibility to arrhythmias. METHODS: The study population included 134 men and 73 women (mean age 61 +/- 14 years) admitted for decompensated CHF. The severity of ventricular arrhythmias was assessed by 24-hour Holter monitoring. None of the patients were on parenteral vasoactive therapy during Holter recording. RESULTS: All measures of ventricular ectopy were markedly lower in women. The average hourly premature ventricular contractions (PVCs), the frequency of ventricular pairs, the mean hourly repetitive ventricular beats, and the frequency of ventricular tachycardia episodes per 24 hours were 40%, 62%, 65%, and 78% lower in women, respectively. Multivariate logistic regression revealed that the risk of developing > 3 ventricular pairs per 24-hour period (OR = 2.2, CI = 1.1-4.2, P = 0.03), > 3 repetitive ventricular beats/hour (OR = 2.5, CI = 1.2-5.3, P = 0.01), or an episode of ventricular tachycardia (OR = 2.1, CI = 1.2-3.9, P = 0.01) were significantly higher in men. Patients in the higher tertile age group had a higher risk for the presence of > 3 ventricular pairs per 24-hour period (OR = 2.3, CI = 1.1-4.2, P = 0.03), and the presence of > 3 repetitive ventricular beats per hour (OR = 5.9, CI = 2.7-13.3, P < 0.0001), compared with patients in the lower age tertile. CONCLUSION: Male sex and age are associated with complex ventricular ectopy in patients with CHF. Further understanding of the mechanisms involved in the relative protection conferred by female sex would advance our understanding about arrhythmias in heart failure.

Age Distribution↗
PubMed2002

New therapies for the treatment of congestive heart failure.

Heart failure is characterized by sodium and fluid retention, sympathetic overactivity, parasympathetic withdrawal, vasoconstrictor activation and cytokine elevation. New therapies for heart failure attempt to control neurohormonal activation and limit progressive left ventricular dysfunction. Nesiritide (human B-type natriuretic peptide) is a recently approved new vasodilator that has been given to almost 1,000 patients in numerous clinical investigations; it belongs to a new class of heart failure drugs known as natriuretic peptides. Nesiritide decreases pulmonary capillary wedge pressure, systemic vascular resistance, mean right atrial pressure and pulmonary artery pressure, while improving cardiac index, stroke volume and heart failure symptoms. Many endothelin receptor antagonists are in various stages of development. Early clinical studies have demonstrated beneficial cardiovascular hemodynamic effects. Other new drugs for heart failure also include calcium sensitizers, neutral endopeptidase and vasopeptidase inhibitors, aldosterone receptor antagonists, vasopressin antagonists and cytokine inhibitors. All are being actively investigated and many show significant promise as beneficial therapies in the treatment of heart failure.

Animals↗
PubMed2002

Nesiritide (Scios).

Nesiritide is a recombinant B-type (brain) natriuretic peptide developed by Scios for the potential treatment of congestive heart failure (CHF). In August 2001, the product was approved and launched in the US for the intravenous treatment of patients with acute decompensated congestive heart failure (ADCHF) who have dyspnea at rest or at minimal activity [418946], [420072]. By March 2002, Scios' European development partner, GlaxoSmithKline, expected to file a Marketing Authorization Application (MAA) for nesiritide in Europe in 2002 [446957].

Journal Article↗
PubMedDate not supplied

A review of the renal and neurohormonal effects of B-type natriuretic peptide.

Adverse neurohormonal activation is an essential component in the pathogenesis of acute decompensated congestive heart failure (CHF). Consequently, blunting this activation is an important therapeutic goal. B-type natriuretic peptide (BNP) is a counterregulatory hormone produced by the ventricles in response to pressure and volume load. Endogenous BNP levels are significantly elevated in patients with acute CHF, but these levels are frequently inadequate to overcome the excess neurohormonal activation present in this condition. Infusion of nesiritide, a recombinant form of endogenous human BNP, increases circulating BNP levels by several-fold, augmenting the counterregulatory effects of this hormone. Clinical trials demonstrate that in patients with acute decompensated CHF, nesiritide produces arterial and venous vasodilation, reducing both preload and afterload; blunts adverse neurohormones, including renin, aldosterone, norepinephrine, and endothelin-1; and improves renal hemodynamics and tubular function. As a result, nesiritide quickly reduces clinical symptoms and improves mortality in patients with acute CHF.

Heart Failure↗