Biography:

In the past Giuseppe Boriani has collaborated on articles with Nazzareno Galié and Alessandro Capucci. One of their most recent publications is Usefulness of nicorandil in congestive heart failure☆. Which was published in journal The American Journal of Cardiology.

More information about Giuseppe Boriani research including statistics on their citations can be found on their Copernicus Academic profile page.

Giuseppe Boriani's Articles: (43)

Usefulness of nicorandil in congestive heart failure☆

AbstractRest and exercise hemodynamic and hormonal effects of nicorandil, a nicotinamide-nitrate vasodilator, were assessed in 9 patients with New York Heart Association class II or III congestive heart failure (CHF) and left ventricular ejection fraction ≤40%. Single oral doses of placebo and 40 and 60 mg of nicorandil were given in a double-blind, randomized trial. Hemodynamic measurements were assessed at rest, up to 8 hours after dose and at peak exercise performed on an upright cycloergometer 1 hour after the dose. Forearm blood flow and venous capacitance were measured by plethysmography 45 minutes after dose. Plasma noradrenaline and plasma renin activity were assessed 1 hour and 2 hours after dose, respectively. Data were analyzed by analysis of variance. Peak effects were observed between 30 and 60 minutes after dose. Mean blood pressure decreased from 86 ± 7 mm Hg after placebo to 78 ± 7 mm Hg after 40 mg (p < 0.05) and to 78 ± 7 mm Hg after 60 mg (p < 0.05) of nicorandil. Mean pulmonary artery pressure decreased from 24 ± 11 to 15 ± 17 mm Hg (p < 0.05) and to 17 ± 7 mm Hg (p < 0.05) and mean pulmonary wedge pressure decreased from 15 ± 8 to 9 ± 4 mm Hg (p < 0.05) and to 10 ± 5 min Hg (p < 0.05). The changes were significant up to 6 to 8 hours after both doses. Cardiac output increased 2 hours after dose from 4.6 ± 0.7 liters/ mm after placebo to 5.5 ± 0.8 liters/min after 60 mg (p < 0.05). At peak exercise mean pulmonary wedge pressure decreased from 29 ± 8 mm Hg after placebo to 24 ± 7 mm Hg (p < 0.05) and to 27 ± 8 mm Hg (difference not significant) after 40 and 60 mg of nicorandil. Venous capacitance increased from 2.9 ± 1.4 ml after placebo to 3.4 ± 1.3 ml after 40 mg of nicorandil (p = 0.1). Cardiac output 1 hour after the meal was 5.7 ± 1 liters/min after placebo and increased to 6.3 ± 1.5 liters/min (p < 0.05) after 40 mg and to 6.2 ± 1 liters/min (p < 0.05) after 60 mg of nicorandil. Plasma renin activity increased from 18.6 ± 29.3 ng/ml/hour after placebo to 24.3 ± 31.1 (p < 0.05) and 22 ± 31.1 ng/ml/hour (p < 0.05) after 40 and 60 mg of nicorandil. Single oral doses of nicorandil in patients with CHF induce favorable changes on rest and exercise hemodynamics up to 6 to 8 hours. An increase of renin activity is also observed.

Effectiveness of loading oral flecainide for converting recent-onset atrial fibrillation to sinus rhythm in patients without organic heart disease or with only systemic hypertension

AbstractSixty-two patients with recent-onset (≤1 week) atrial fibrillation (New York Heart Association functional class 1 and 2) were randomized in a single-blind study to 1 of the following treatment groups: (1) flecainide (300 mg) as a single oral loading dose; or (2) amiodarone (5 mg/kg) as an intravenous bolus, followed by 1.8 g/day; or (3) placebo for the first 8 hours. Twenty-four-hour Holter recording was performed, and conversion to sinus rhythm at 3, 8, 12 and 24 hours was considered as the criterion of efficacy. Conversion to sinus rhythm was achieved within 8 hours (placebo-controlled period) in 20 of 22 patients (91%) treated with flecainide, 7 of 19 (37%) treated with amiodarone (p < 0.001 vs flecainide), and 10 of 21 (48%) treated with placebo (p < 0.01 vs flecainide). Resumption of sinus rhythm within 24 hours occurred in 21 of 22 patients (95%) with flecainide and in 17 of 19 (89%) with amiodarone (p = not significant). Mean conversion times were shorter for flecainide (190 ± 147 minutes) than for amiodarone (705 ± 418; p < 0.001). No major side effects occurred. At Holter monitoring, a pause of 9.3 seconds was observed in 1 asymptomatic patient treated with flecainide. Phases of atrial flutter with a ventricular rate ≤150 beats/ min were detected before sinus conversion in 1 patient receiving placebo and in 2 receiving flecainide. In conclusion, flecainide administered orally in a single loading dose is highly effective in converting recent-onset atrial fibrilation to sinus rhythm and is more rapid than is intravenous amiodarone. This in-hospital regimen in patients without major organic heart diseases was safe and well-tolerated.

Usefulness of nicorandil in congestive heart failure☆

AbstractRest and exercise hemodynamic and hormonal effects of nicorandil, a nicotinamide-nitrate vasodilator, were assessed in 9 patients with New York Heart Association class II or III congestive heart failure (CHF) and left ventricular ejection fraction ≤40%. Single oral doses of placebo and 40 and 60 mg of nicorandil were given in a double-blind, randomized trial. Hemodynamic measurements were assessed at rest, up to 8 hours after dose and at peak exercise performed on an upright cycloergometer 1 hour after the dose. Forearm blood flow and venous capacitance were measured by plethysmography 45 minutes after dose. Plasma noradrenaline and plasma renin activity were assessed 1 hour and 2 hours after dose, respectively. Data were analyzed by analysis of variance. Peak effects were observed between 30 and 60 minutes after dose. Mean blood pressure decreased from 86 ± 7 mm Hg after placebo to 78 ± 7 mm Hg after 40 mg (p < 0.05) and to 78 ± 7 mm Hg after 60 mg (p < 0.05) of nicorandil. Mean pulmonary artery pressure decreased from 24 ± 11 to 15 ± 17 mm Hg (p < 0.05) and to 17 ± 7 mm Hg (p < 0.05) and mean pulmonary wedge pressure decreased from 15 ± 8 to 9 ± 4 mm Hg (p < 0.05) and to 10 ± 5 min Hg (p < 0.05). The changes were significant up to 6 to 8 hours after both doses. Cardiac output increased 2 hours after dose from 4.6 ± 0.7 liters/ mm after placebo to 5.5 ± 0.8 liters/min after 60 mg (p < 0.05). At peak exercise mean pulmonary wedge pressure decreased from 29 ± 8 mm Hg after placebo to 24 ± 7 mm Hg (p < 0.05) and to 27 ± 8 mm Hg (difference not significant) after 40 and 60 mg of nicorandil. Venous capacitance increased from 2.9 ± 1.4 ml after placebo to 3.4 ± 1.3 ml after 40 mg of nicorandil (p = 0.1). Cardiac output 1 hour after the meal was 5.7 ± 1 liters/min after placebo and increased to 6.3 ± 1.5 liters/min (p < 0.05) after 40 mg and to 6.2 ± 1 liters/min (p < 0.05) after 60 mg of nicorandil. Plasma renin activity increased from 18.6 ± 29.3 ng/ml/hour after placebo to 24.3 ± 31.1 (p < 0.05) and 22 ± 31.1 ng/ml/hour (p < 0.05) after 40 and 60 mg of nicorandil. Single oral doses of nicorandil in patients with CHF induce favorable changes on rest and exercise hemodynamics up to 6 to 8 hours. An increase of renin activity is also observed.

Effectiveness of loading oral flecainide for converting recent-onset atrial fibrillation to sinus rhythm in patients without organic heart disease or with only systemic hypertension

AbstractSixty-two patients with recent-onset (≤1 week) atrial fibrillation (New York Heart Association functional class 1 and 2) were randomized in a single-blind study to 1 of the following treatment groups: (1) flecainide (300 mg) as a single oral loading dose; or (2) amiodarone (5 mg/kg) as an intravenous bolus, followed by 1.8 g/day; or (3) placebo for the first 8 hours. Twenty-four-hour Holter recording was performed, and conversion to sinus rhythm at 3, 8, 12 and 24 hours was considered as the criterion of efficacy. Conversion to sinus rhythm was achieved within 8 hours (placebo-controlled period) in 20 of 22 patients (91%) treated with flecainide, 7 of 19 (37%) treated with amiodarone (p < 0.001 vs flecainide), and 10 of 21 (48%) treated with placebo (p < 0.01 vs flecainide). Resumption of sinus rhythm within 24 hours occurred in 21 of 22 patients (95%) with flecainide and in 17 of 19 (89%) with amiodarone (p = not significant). Mean conversion times were shorter for flecainide (190 ± 147 minutes) than for amiodarone (705 ± 418; p < 0.001). No major side effects occurred. At Holter monitoring, a pause of 9.3 seconds was observed in 1 asymptomatic patient treated with flecainide. Phases of atrial flutter with a ventricular rate ≤150 beats/ min were detected before sinus conversion in 1 patient receiving placebo and in 2 receiving flecainide. In conclusion, flecainide administered orally in a single loading dose is highly effective in converting recent-onset atrial fibrilation to sinus rhythm and is more rapid than is intravenous amiodarone. This in-hospital regimen in patients without major organic heart diseases was safe and well-tolerated.

Usefulness of nicorandil in congestive heart failure☆

AbstractRest and exercise hemodynamic and hormonal effects of nicorandil, a nicotinamide-nitrate vasodilator, were assessed in 9 patients with New York Heart Association class II or III congestive heart failure (CHF) and left ventricular ejection fraction ≤40%. Single oral doses of placebo and 40 and 60 mg of nicorandil were given in a double-blind, randomized trial. Hemodynamic measurements were assessed at rest, up to 8 hours after dose and at peak exercise performed on an upright cycloergometer 1 hour after the dose. Forearm blood flow and venous capacitance were measured by plethysmography 45 minutes after dose. Plasma noradrenaline and plasma renin activity were assessed 1 hour and 2 hours after dose, respectively. Data were analyzed by analysis of variance. Peak effects were observed between 30 and 60 minutes after dose. Mean blood pressure decreased from 86 ± 7 mm Hg after placebo to 78 ± 7 mm Hg after 40 mg (p < 0.05) and to 78 ± 7 mm Hg after 60 mg (p < 0.05) of nicorandil. Mean pulmonary artery pressure decreased from 24 ± 11 to 15 ± 17 mm Hg (p < 0.05) and to 17 ± 7 mm Hg (p < 0.05) and mean pulmonary wedge pressure decreased from 15 ± 8 to 9 ± 4 mm Hg (p < 0.05) and to 10 ± 5 min Hg (p < 0.05). The changes were significant up to 6 to 8 hours after both doses. Cardiac output increased 2 hours after dose from 4.6 ± 0.7 liters/ mm after placebo to 5.5 ± 0.8 liters/min after 60 mg (p < 0.05). At peak exercise mean pulmonary wedge pressure decreased from 29 ± 8 mm Hg after placebo to 24 ± 7 mm Hg (p < 0.05) and to 27 ± 8 mm Hg (difference not significant) after 40 and 60 mg of nicorandil. Venous capacitance increased from 2.9 ± 1.4 ml after placebo to 3.4 ± 1.3 ml after 40 mg of nicorandil (p = 0.1). Cardiac output 1 hour after the meal was 5.7 ± 1 liters/min after placebo and increased to 6.3 ± 1.5 liters/min (p < 0.05) after 40 mg and to 6.2 ± 1 liters/min (p < 0.05) after 60 mg of nicorandil. Plasma renin activity increased from 18.6 ± 29.3 ng/ml/hour after placebo to 24.3 ± 31.1 (p < 0.05) and 22 ± 31.1 ng/ml/hour (p < 0.05) after 40 and 60 mg of nicorandil. Single oral doses of nicorandil in patients with CHF induce favorable changes on rest and exercise hemodynamics up to 6 to 8 hours. An increase of renin activity is also observed.

Effectiveness of loading oral flecainide for converting recent-onset atrial fibrillation to sinus rhythm in patients without organic heart disease or with only systemic hypertension

AbstractSixty-two patients with recent-onset (≤1 week) atrial fibrillation (New York Heart Association functional class 1 and 2) were randomized in a single-blind study to 1 of the following treatment groups: (1) flecainide (300 mg) as a single oral loading dose; or (2) amiodarone (5 mg/kg) as an intravenous bolus, followed by 1.8 g/day; or (3) placebo for the first 8 hours. Twenty-four-hour Holter recording was performed, and conversion to sinus rhythm at 3, 8, 12 and 24 hours was considered as the criterion of efficacy. Conversion to sinus rhythm was achieved within 8 hours (placebo-controlled period) in 20 of 22 patients (91%) treated with flecainide, 7 of 19 (37%) treated with amiodarone (p < 0.001 vs flecainide), and 10 of 21 (48%) treated with placebo (p < 0.01 vs flecainide). Resumption of sinus rhythm within 24 hours occurred in 21 of 22 patients (95%) with flecainide and in 17 of 19 (89%) with amiodarone (p = not significant). Mean conversion times were shorter for flecainide (190 ± 147 minutes) than for amiodarone (705 ± 418; p < 0.001). No major side effects occurred. At Holter monitoring, a pause of 9.3 seconds was observed in 1 asymptomatic patient treated with flecainide. Phases of atrial flutter with a ventricular rate ≤150 beats/ min were detected before sinus conversion in 1 patient receiving placebo and in 2 receiving flecainide. In conclusion, flecainide administered orally in a single loading dose is highly effective in converting recent-onset atrial fibrilation to sinus rhythm and is more rapid than is intravenous amiodarone. This in-hospital regimen in patients without major organic heart diseases was safe and well-tolerated.

Usefulness of nicorandil in congestive heart failure☆

AbstractRest and exercise hemodynamic and hormonal effects of nicorandil, a nicotinamide-nitrate vasodilator, were assessed in 9 patients with New York Heart Association class II or III congestive heart failure (CHF) and left ventricular ejection fraction ≤40%. Single oral doses of placebo and 40 and 60 mg of nicorandil were given in a double-blind, randomized trial. Hemodynamic measurements were assessed at rest, up to 8 hours after dose and at peak exercise performed on an upright cycloergometer 1 hour after the dose. Forearm blood flow and venous capacitance were measured by plethysmography 45 minutes after dose. Plasma noradrenaline and plasma renin activity were assessed 1 hour and 2 hours after dose, respectively. Data were analyzed by analysis of variance. Peak effects were observed between 30 and 60 minutes after dose. Mean blood pressure decreased from 86 ± 7 mm Hg after placebo to 78 ± 7 mm Hg after 40 mg (p < 0.05) and to 78 ± 7 mm Hg after 60 mg (p < 0.05) of nicorandil. Mean pulmonary artery pressure decreased from 24 ± 11 to 15 ± 17 mm Hg (p < 0.05) and to 17 ± 7 mm Hg (p < 0.05) and mean pulmonary wedge pressure decreased from 15 ± 8 to 9 ± 4 mm Hg (p < 0.05) and to 10 ± 5 min Hg (p < 0.05). The changes were significant up to 6 to 8 hours after both doses. Cardiac output increased 2 hours after dose from 4.6 ± 0.7 liters/ mm after placebo to 5.5 ± 0.8 liters/min after 60 mg (p < 0.05). At peak exercise mean pulmonary wedge pressure decreased from 29 ± 8 mm Hg after placebo to 24 ± 7 mm Hg (p < 0.05) and to 27 ± 8 mm Hg (difference not significant) after 40 and 60 mg of nicorandil. Venous capacitance increased from 2.9 ± 1.4 ml after placebo to 3.4 ± 1.3 ml after 40 mg of nicorandil (p = 0.1). Cardiac output 1 hour after the meal was 5.7 ± 1 liters/min after placebo and increased to 6.3 ± 1.5 liters/min (p < 0.05) after 40 mg and to 6.2 ± 1 liters/min (p < 0.05) after 60 mg of nicorandil. Plasma renin activity increased from 18.6 ± 29.3 ng/ml/hour after placebo to 24.3 ± 31.1 (p < 0.05) and 22 ± 31.1 ng/ml/hour (p < 0.05) after 40 and 60 mg of nicorandil. Single oral doses of nicorandil in patients with CHF induce favorable changes on rest and exercise hemodynamics up to 6 to 8 hours. An increase of renin activity is also observed.

Effectiveness of loading oral flecainide for converting recent-onset atrial fibrillation to sinus rhythm in patients without organic heart disease or with only systemic hypertension

AbstractSixty-two patients with recent-onset (≤1 week) atrial fibrillation (New York Heart Association functional class 1 and 2) were randomized in a single-blind study to 1 of the following treatment groups: (1) flecainide (300 mg) as a single oral loading dose; or (2) amiodarone (5 mg/kg) as an intravenous bolus, followed by 1.8 g/day; or (3) placebo for the first 8 hours. Twenty-four-hour Holter recording was performed, and conversion to sinus rhythm at 3, 8, 12 and 24 hours was considered as the criterion of efficacy. Conversion to sinus rhythm was achieved within 8 hours (placebo-controlled period) in 20 of 22 patients (91%) treated with flecainide, 7 of 19 (37%) treated with amiodarone (p < 0.001 vs flecainide), and 10 of 21 (48%) treated with placebo (p < 0.01 vs flecainide). Resumption of sinus rhythm within 24 hours occurred in 21 of 22 patients (95%) with flecainide and in 17 of 19 (89%) with amiodarone (p = not significant). Mean conversion times were shorter for flecainide (190 ± 147 minutes) than for amiodarone (705 ± 418; p < 0.001). No major side effects occurred. At Holter monitoring, a pause of 9.3 seconds was observed in 1 asymptomatic patient treated with flecainide. Phases of atrial flutter with a ventricular rate ≤150 beats/ min were detected before sinus conversion in 1 patient receiving placebo and in 2 receiving flecainide. In conclusion, flecainide administered orally in a single loading dose is highly effective in converting recent-onset atrial fibrilation to sinus rhythm and is more rapid than is intravenous amiodarone. This in-hospital regimen in patients without major organic heart diseases was safe and well-tolerated.

Usefulness of nicorandil in congestive heart failure☆

AbstractRest and exercise hemodynamic and hormonal effects of nicorandil, a nicotinamide-nitrate vasodilator, were assessed in 9 patients with New York Heart Association class II or III congestive heart failure (CHF) and left ventricular ejection fraction ≤40%. Single oral doses of placebo and 40 and 60 mg of nicorandil were given in a double-blind, randomized trial. Hemodynamic measurements were assessed at rest, up to 8 hours after dose and at peak exercise performed on an upright cycloergometer 1 hour after the dose. Forearm blood flow and venous capacitance were measured by plethysmography 45 minutes after dose. Plasma noradrenaline and plasma renin activity were assessed 1 hour and 2 hours after dose, respectively. Data were analyzed by analysis of variance. Peak effects were observed between 30 and 60 minutes after dose. Mean blood pressure decreased from 86 ± 7 mm Hg after placebo to 78 ± 7 mm Hg after 40 mg (p < 0.05) and to 78 ± 7 mm Hg after 60 mg (p < 0.05) of nicorandil. Mean pulmonary artery pressure decreased from 24 ± 11 to 15 ± 17 mm Hg (p < 0.05) and to 17 ± 7 mm Hg (p < 0.05) and mean pulmonary wedge pressure decreased from 15 ± 8 to 9 ± 4 mm Hg (p < 0.05) and to 10 ± 5 min Hg (p < 0.05). The changes were significant up to 6 to 8 hours after both doses. Cardiac output increased 2 hours after dose from 4.6 ± 0.7 liters/ mm after placebo to 5.5 ± 0.8 liters/min after 60 mg (p < 0.05). At peak exercise mean pulmonary wedge pressure decreased from 29 ± 8 mm Hg after placebo to 24 ± 7 mm Hg (p < 0.05) and to 27 ± 8 mm Hg (difference not significant) after 40 and 60 mg of nicorandil. Venous capacitance increased from 2.9 ± 1.4 ml after placebo to 3.4 ± 1.3 ml after 40 mg of nicorandil (p = 0.1). Cardiac output 1 hour after the meal was 5.7 ± 1 liters/min after placebo and increased to 6.3 ± 1.5 liters/min (p < 0.05) after 40 mg and to 6.2 ± 1 liters/min (p < 0.05) after 60 mg of nicorandil. Plasma renin activity increased from 18.6 ± 29.3 ng/ml/hour after placebo to 24.3 ± 31.1 (p < 0.05) and 22 ± 31.1 ng/ml/hour (p < 0.05) after 40 and 60 mg of nicorandil. Single oral doses of nicorandil in patients with CHF induce favorable changes on rest and exercise hemodynamics up to 6 to 8 hours. An increase of renin activity is also observed.

Effectiveness of loading oral flecainide for converting recent-onset atrial fibrillation to sinus rhythm in patients without organic heart disease or with only systemic hypertension

AbstractSixty-two patients with recent-onset (≤1 week) atrial fibrillation (New York Heart Association functional class 1 and 2) were randomized in a single-blind study to 1 of the following treatment groups: (1) flecainide (300 mg) as a single oral loading dose; or (2) amiodarone (5 mg/kg) as an intravenous bolus, followed by 1.8 g/day; or (3) placebo for the first 8 hours. Twenty-four-hour Holter recording was performed, and conversion to sinus rhythm at 3, 8, 12 and 24 hours was considered as the criterion of efficacy. Conversion to sinus rhythm was achieved within 8 hours (placebo-controlled period) in 20 of 22 patients (91%) treated with flecainide, 7 of 19 (37%) treated with amiodarone (p < 0.001 vs flecainide), and 10 of 21 (48%) treated with placebo (p < 0.01 vs flecainide). Resumption of sinus rhythm within 24 hours occurred in 21 of 22 patients (95%) with flecainide and in 17 of 19 (89%) with amiodarone (p = not significant). Mean conversion times were shorter for flecainide (190 ± 147 minutes) than for amiodarone (705 ± 418; p < 0.001). No major side effects occurred. At Holter monitoring, a pause of 9.3 seconds was observed in 1 asymptomatic patient treated with flecainide. Phases of atrial flutter with a ventricular rate ≤150 beats/ min were detected before sinus conversion in 1 patient receiving placebo and in 2 receiving flecainide. In conclusion, flecainide administered orally in a single loading dose is highly effective in converting recent-onset atrial fibrilation to sinus rhythm and is more rapid than is intravenous amiodarone. This in-hospital regimen in patients without major organic heart diseases was safe and well-tolerated.

Trial DesignThe MINERVA study design and rationale: A controlled randomized trial to assess the clinical benefit of minimizing ventricular pacing in pacemaker patients with atrial tachyarrhythmias

BackgroundDual-chamber (DDD) pacing has generally been regarded as “physiologic pacing” and therefore expected to be superior to ventricular pacing. Major randomized trials have so far failed to demonstrate significant reductions in the incidences of mortality, stroke, and heart failure. It has been shown that unnecessary ventricular pacing in patients with sinus node dysfunction or only intermittent atrioventricular block is associated with ventricular desynchronization and increased risk of atrial tachyarrhythmias (ATA).MethodsThe MINimizE Right Ventricular pacing to prevent Atrial fibrillation and heart failure (MINERVA) study is a prospective, multi-center, randomized, international, single-blind, controlled trial designed to determine whether physiologic pacing through the managed ventricular pacing (MVP) algorithm combined with preventive atrial pacing (PAP) and atrial antitachycardia pacing (ATP) is superior to standard DDD pacing in terms of 2-year reduction in death, permanent ATA, and cardiovascular hospitalizations. Patients with standard class I or II indications for permanent DDD pacing and history of ATA will receive a Medtronic EnRhythm implantable pacemaker (Medtronic, Minneapolis, MN). After a 1-month run-in period, patients will be randomized in a 1:1:1 manner to the DDD (control group, all OFF), the DDDRP (MVP + PAP + ATP ON), and the MVP group (only MVP ON). Up to 1,300 patients will be included in approximately 70 centers in Europe, the Middle East, and Asia.ConclusionsThe MINERVA study will make an important contribution to the management of patients with paroxysmal ATA and accepted indications for dual-chamber pacemaker implantation by determining whether physiologic pacing combined with PAP and ATP is superior to standard DDD pacing in terms of reduction of mortality, incidence of permanent ATA, and cardiovascular hospitalizations.

Clinical InvestigationImpact of chronic obstructive pulmonary disease on prognosis in atrial fibrillation: A report from the EURObservational Research Programme Pilot Survey on Atrial Fibrillation (EORP-AF) General Registry

BackgroundChronic obstructive pulmonary disease (COPD) is a common chronic disease, being associated with both high rates of morbidity and mortality. Similarly, atrial fibrillation (AF) is associated with a higher risk of both cardiovascular (CV) events and overall mortality. The AF and COPD often coexist, but the impact of COPD on prognosis in European AF patients is unknown.MethodsWe evaluated COPD prevalence in patients enrolled in the EURObservational Research Programme Pilot Survey on Atrial Fibrillation Registry Pilot Phase. Clinical factors associated with COPD and adverse outcomes at 1-year follow-up were determined.ResultsIn the overall cohort, a diagnosis of COPD was recorded in 339 (11.0%) of AF patients. The AF patients with COPD were more burdened with risk factors and comorbidities, including diabetes mellitus (P < .0001) and chronic heart failure (P < .0001). β-Blockers were less likely to be prescribed to patients with COPD (P = .0007). On follow-up, AF patients with COPD had a higher risk of both CV death and all-cause death (both P < .0001), as well as for the composite outcome of any thromboembolic event/bleeding /CV death (P = .0003). Cox regression analysis found that COPD was independently associated with an increase in all-cause death (hazard ratio, 1.55; 95% CI 1.05-2.28; P = .0269).ConclusionsChronic obstructive pulmonary disease is highly prevalent in European AF patients, and is associated with higher rates of CV death, all-cause death, and the composite outcome of any thromboembolic event/bleeding/CV death. The presence of COPD in AF patients was independently associated with all-cause death in AF patients.

Coronary artery diseaseTroponin I Rise After Pacemaker Implantation at the Time of “Universal Definition of Myocardial Infarction”

We assessed incidence, magnitude, and time course of cardiac troponin I (cTnI) increase after pacemaker implantation in patients without acute coronary syndromes (ACSs). Seventy patients (mean age 71 years, interquartile range 44 to 92, 38 men) undergoing elective implantation of a single-/dual-chamber pacemaker with active/passive fixation leads were enrolled, excluding subjects with clinical suspicion of ACS, abnormal basal cTnI level, or presenting conditions predisposing to abnormal cTnI. Cardiac TnI concentrations were determined in basal conditions, at the end of the procedure, and after 8, 12, and 24 hours. Single-/dual-chamber devices were implanted in 31 of 39 patients. Cardiac TnI peak concentration occurred within the 12-hour assay in 69 of 70 patients; 26 of 70 had a cTnI above the normal cut-off range. All patients presented normal cTnI at 24-hour assay. In conclusion, pacemaker implantation is associated with increases of cTnI levels in up to 37% of patients. This can affect the specificity of cTnI assessment for ruling out ACS, especially within 12 hours after the procedure. These data deserve consideration in a contemporary setting, in which troponin has gathered a pivotal role in the diagnosis and therapy of ACS, and in particular clinical presentations in which electrocardiogram loses its diagnostic capabilities (due to paced rhythms) and symptoms may be lacking or confusing.

Heart failureRadionuclide Angiographic Determination of Regional Left Ventricular Systolic Function During Rest and Exercise in Patients With Nonischemic Cardiomyopathy Treated With Cardiac Resynchronization Therapy

Cardiac resynchronization therapy (CRT) can improve global left ventricular (LV) function. However, limited data are available on regional LV contractility at rest and during exercise. The aim of the present study was to prospectively investigate the effects of CRT on regional LV ejection fraction (EF), global LVEF, and dyssynchrony, during rest and exercise, using radionuclide angiography. A total of 32 consecutive patients with heart failure and nonischemic cardiomyopathy underwent technetium-99m radionuclide angiography with bicycle exercise immediately after CRT implantation (during spontaneous rhythm and after CRT activation) and 3 months later. The regional EF was assessed in the interventricular septum and the lateral wall (LW). Intraventricular dyssynchrony was evaluated using Fourier phase analysis. During spontaneous rhythm, the EF was severely depressed in the septum compared to in the LW. CRT improved septal EF at rest and during exercise both at baseline (p <0.001) and after 3 months (p <0.05). The basal LW EF decreased during CRT (p <0.05, both at rest and during exercise). LV dyssynchrony decreased both at baseline and during follow-up, and the global LVEF showed improvement only at 3 months (p <0.001). In conclusion, in patients with nonischemic cardiomyopathy, CRT affects regional LV function by increasing the septal EF and reducing LW contractility, both at rest and during exercise. This was associated with an improvement in global LVEF and dyssynchrony.

Clinical InvestigationsCardiologyLeft Superior Vena Cava Persistence in Patients Undergoing Pacemaker or Cardioverter-Defibrillator Implantation: A 10-Year Experience

ObjectiveThe persistence of a left superior vena cava(LSVC) has been observed in 0.3% of the general population asestablished by autopsy. In the adult population, it is an importantanatomic finding if a left superior approach to the heart isconsidered. The aim of the study was to evaluate the prevalence of aLSVC in patients undergoing pacemaker (PM) andcardioverter-defibrillator (CD) implantation.DesignWe observed the prevalence of LSVC during a 10-year period; eachpatient undergoing PM or transvenous CD implantation received a leftcephalic/left subclavian venous approach to the heart. With thistechnique, LSVC persistence is easily diagnosed during leadplacement.ResultsA total of 1,139 patientsconsecutively underwent PM implantation during 10 years: 4 patients hadpersistent LSCV (0.34%). Among 115 patients undergoing CDimplantation, 2 patients with LSVC (1.7%) were observed. Overall LSVCpersistence was found in 6 of 1,254 patients (0.47%). Two patients, one of whom had no right superior vena cava (RSVC), received aleft-sided PM, whereas two other patients received right-sided devices. Both CD patients received a left-sided active-can device: the firstpatient with a right-sided lead tunneled to the left pectoral pocket, as a result of poor catheter handling through the LSVC and coronarysinus, and the second patient with a screw-in lead from LSVC. Long-termfollow-up of these patients (average ± SD, 41 ± 26 months)revealed absence of lead dislodgment and appropriate device functionregardless of lead implantation site.ConclusionsPersistence of LSVC in adults undergoing PM/CD implantation is similarto that of the general population (0.47% in our study). The left-sidedimplant can be achieved by stylet shaping and by use of active fixationleads in most patients, with a reliable outcome at short term inaddition to appropriate device performance at follow-up. Assessment ofthe RSVC is advisable when planning a right-sided implantation, since aminority of patients lacks this vessel.

Clinical Investigations; Articles; CardiologyPropafenone for Conversion of Recent-Onset Atrial Fibrillation: A Controlled Comparison Between Oral Loading Dose and Intravenous Administration

Study objectiveTo compare placebo vs two different regimens of propafenone administration—intravenous administration or short-term oral loading—in converting recent-onset atrial fibrillation to sinus rhythm.DesignSingle-blind placebo-controlled study.PatientsEighty-seven patients with atrial fibrillation of recent onset (≤7 days' duration) admitted to the hospital without signs of organic heart disease (n=42) or with systemic hypertension without signs or symptoms of heart failure (n=45). The patients were assigned randomly to treatment with intravenous propafenone (29 patients), oral propafenone (29 patients), or placebo (29 patients).InterventionsAdministration of propafenone intravenously (2-mg/kg bolus followed by 0.0078 mg/kg/min) or as short-term oral loading (600 mg orally single dose). Patients were submitted to Holter monitoring and conversion to sinus rhythm was evaluated at 1, 3, and 8 h.ResultsConversion to sinus rhythm was obtained within 1 h in 28% with intravenous propafenone, in 3% with oral propafenone, and in 3% with placebo. At 3 h, the efficacy of intravenous propafenone (41%) and of oral propafenone (55%) were statistically superior to placebo (10% of conversions) and at 8 h either intravenous or oral propafenone were effective in almost two thirds of the patients with a statistical difference vs placebo, whose efficacy was 24%. No major side effects were observed.ConclusionsPropafenone as an oral loading dose is an efficacious and fast way of treating atrial fibrillation of recent onset and due to its simplicity of administration and safety can be preferred to the intravenous route.(CHEST 1995; 108:355-58)

Clinical Investigations: CardiologyEvaluation of Myocardial Injury Following Repeated Internal Atrial Shocks by Monitoring Serum Cardiac Troponin I Levels

IntroductionElectrical shocks delivered for atrial cardioversion (CV) may cause myocardial damage. The aim of this study was to assess the extent of myocardial injury caused by repeated intracardiac shocks delivered for low-energy internal atrial CV.Methods and resultsThirty-five patients with chronic persistent atrial fibrillation (AF) of different etiologies underwent CV with delivery of synchronized biphasic shocks (3.0/3.0 ms) between two catheters positioned in the right atrium and the coronary sinus. Shocks were delivered according to a step-up protocol (50 V, 180 V, then steps of 40 to 56 V up to 500 V, if necessary). In 23 patients, AF was reinduced after baseline CV, and CV was repeated. Myocardial injury was monitored by measuring cardiac troponin I (cTnI) serum concentrations in blood samples taken at baseline and at 2, 4, 8, 12, and 24 h after the procedure, by means of an immunoenzymologic assay (normal values, ≤ 0.6 ng/mL). A mean (± SD) of 6.9 ± 3.4 shocks per patient were delivered (range, 2 to 17). Shocks delivered in each patient had a maximal energy of 7.3 ± 4.0 J (range, 1.7 to 15.7). In 20 patients (57%), no evidence of myocardial injury (cTnI level, ≤ 0.6 ng/mL) was found. In 13 patients (37%), mildly elevated cTnI levels (range, 0.7 to 1.4 ng/mL) in samples taken 4 to 12 h after CV suggested minor myocardial injury. In two patients (6%), higher cTnI levels were found in samples taken 4 to 8 h after CV (peak, 1.7 and 2.4 ng/mL), indicating a necrotic damage. Patients with no cTnI elevation, with mild cTnI elevation, or with cTnI levels≥ 1.5 ng/mL did not differ significantly with respect to the total number of shocks delivered, the mean amount of energy delivered, and the cumulative amount of energy delivered. No clinical complications were observed.ConclusionsFollowing internal CV with the delivery of repeated shocks, minor elevations of cTnI serum levels could be detected in a significant proportion of patients, and this suggests subtle asymptomatic minor myocardial injury. The elevations of cTnI levels do not appear to be related to the number of shocks or to the amount of energy delivered.

Case ReportAgainst all odds: Targeted pacing site for resynchronization therapy by venoplasty and active fixation lead

AbstractIn cardiac resynchronization therapy, reaching the target pacing site is essential to achieve optimal therapy. Coronary vein stenosis in the target vein might be an obstacle for lead placement, which can be overcome by venoplasty and stenting of the narrowed segment. Additional active fixation of the left ventricular lead ensures precise location in the target site with minimal risk of lead dislodgment.

Efficacy of internal cardioversion for chronic atrial fibrillation in patients with and without left ventricular dysfunction

AbstractInternal cardioversion can restore sinus rhythm with energies below 6–10 J, often without anaesthesia/sedation. We investigated its safety and short-/medium-term efficacy in patients with persistent atrial fibrillation (AF) with left ventricular dysfunction (defined as ejection fraction ≤40%). Among 34 patients with persistent AF who agreed to receive internal cardioversion, 16 had left ventricular dysfunction and 18 did not (the groups were similar as regards age, duration of AF and pretreatment with amiodarone). Internal CV was performed delivering 3.0/3.0-ms biphasic shocks between coil catheters using a step-up protocol. Sinus rhythm was always restored. General anaesthesia (administered only when discomfort was not tolerated) was required only in 2 of the 16 (12.5%) patients with left ventricular dysfunction. The defibrillation threshold was similar in patients with and without left ventricular dysfunction (10.2±6.9 vs. 8.4±4.9 J; p=0.37). Short-term (within 72 h) AF recurrence rates in the presence and absence of left ventricular dysfunction were 19% (3/16) and 6% (1/18), respectively (p=0.51). After cardioversion, all patients received antiarrhythmic drugs (mostly amiodarone in patients with left ventricular dysfunction and class IC agents in the remainder). With mean follow-up periods of about 220 days, AF recurrence rates among patients with and without left ventricular dysfunction were 50% (8/16) and 28% (5/18), respectively (p=0.328). We conclude that even in patients with left ventricular dysfunction, internal CV is safe and effective, minimizing risks from anaesthesia. Although these patients may have a higher risk of short- or medium-term AF recurrence, 6-month maintenance of sinus rhythm is possible in about 50% of cases.

Heart failure after myocardial revascularization: Risk markers

AbstractWe investigated the prognostic weight of several risk factors for heart failure in patients undergoing CABG. We followed 351 consecutive patients for 18±12 months after surgery to assess clinical outcome, presence and degree of heart failure. The risk of developing heart failure >class 2 at 1 year was investigated by logistic regression on the following preoperative variables: sex, age, left ventricular EF, QRS duration, previous MI, history of heart failure, atrial fibrillation (AF), hypertension, hypercholesterolemia, diabetes, previous stroke.Age was 70±8 years and EF was 54±12% at the time of surgery. Heart failure >class 2 occurred in 95/351 patients (27%) at follow up. Logistic regression identified QRS duration (OR=1.02), a history of stroke (OR=3.94), and diabetes (OR=1.98) as predictors of CHF at follow up. All the other variables were not risk markers for heart failure at logistic regression.Thirty five patients (10%) had QRS≥140 ms before surgery; 51% of them had CHF at follow up compared to 24% of patients with QRS<140 ms (p<0.05).In the current surgical era, candidates to CABG (50% of patients older than 70 years) have a relevant likelihood of heart failure at follow up, despite myocardial revascularization. Risk stratification may rely upon inexpensive variables as previous stroke, diabetes, and QRS duration. A minority of patients (5%) could benefit from LV-based pacing, which should be considered at the same surgical time via an epicardial implantation.

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