enalapril and Tachycardia--Paroxysmal

Angiotensin II and aldosterone are key factors responsible for the structural and neurohormonal remodeling of the atria and ventricles in patients with atrial fibrillation (AF). The aim of the present study was to evaluate the antiarrhythmic effects of spironolactone compared to angiotensin-converting enzyme inhibitors in patients with recurrent AF. A cohort of 164 consecutive patients (mean age 66 years, 87 men), with an average 4-year history of recurrent AF episodes, was enrolled in a prospective, randomized, 12-month trial with 4 treatment arms: group A, spironolactone, enalapril, and a β blocker; group B, spironolactone and a β blocker; group C, enalapril plus a β blocker; and group D, a β blocker alone. The primary end point of the trial was the presence of symptomatic AF episodes documented on the electrocardiogram. At 3-, 6-, 9-, and 12 months, a significant (p < 0.001) reduction had occurred in the incidence of AF episodes in both spironolactone-treated groups (group A, spironolactone, enalapril, and a β blocker; and group B, spironolactone plus a β blocker) compared to the incidence in patients treated with enalapril and a β blocker (group C) or a β blocker alone (group D). No significant difference was seen in AF recurrences between patients taking spironolactone and a β blocker with (group A) and without (group B) enalapril. No significant differences were found in the systolic or diastolic blood pressure or heart rate among the groups before and after 1 year of follow-up. In conclusion, combined spironolactone plus β-blocker treatment might be a simple and valuable option in preventing AF episodes in patients with normal left ventricular function and a history of refractory paroxysmal AF.

Topics: Adrenergic beta-Antagonists; Aged; Angiotensin-Converting Enzyme Inhibitors; Atrial Fibrillation; Blood Pressure; Dose-Response Relationship, Drug; Drug Therapy, Combination; Electrocardiography; Enalapril; Female; Follow-Up Studies; Heart Rate; Humans; Male; Mineralocorticoid Receptor Antagonists; Prospective Studies; Spironolactone; Tachycardia, Paroxysmal; Treatment Outcome

The purpose of this study was to examine the relationship between long-term efficacy of amiodarone therapy (100-200 mg/day) combined with angiotensin converting enzyme inhibitor (ACEI; enalapril 5 mg/day) administration, and the development of structural atrial remodeling in patients with paroxysmal atrial fibrillation (AF). Fifty-eight patients (40 men, 18 women, mean age, 68 +/- 8 years, mean follow-up period, 43 +/- 18 months) with AF refractory to >or= two class I antiarrhythmic drugs were divided into two groups; those treated with enalapril on amiodarone (group A, n = 25) and those treated with amiodarone alone (group B, n = 33), to evaluate the efficacy of combination therapy. 1) At 12 and 24 months, the survival rates for patients free from AF recurrence were 80% and 64% in group A, and 45% and 30% in group B, respectively (P < 0.05, group A versus group B). The percentage of patients with conversion to permanent AF despite amiodarone therapy was 20% in group A and 48.5% in group B (P < 0.05, group A versus group B). 2) In group B, left atrial dimension (LAD) was significantly greater after amiodarone therapy (40.2 +/- 6.3 mm) than at baseline (35.2 +/- 6.6 mm) (P < 0.01), whereas there was no significant difference in LAD between baseline and after amiodarone therapy in group A (39.1 +/- 5.0 mm versus 41.0 +/- 5.0 mm, respectively). In patients with paroxysmal AF, ACE-I appears to enhance the efficacy of amiodarone therapy in maintaining sinus rhythm and preventing the development of structural remodeling in atria.

Topics: Aged; Amiodarone; Angiotensin-Converting Enzyme Inhibitors; Anti-Arrhythmia Agents; Atrial Fibrillation; Drug Therapy, Combination; Echocardiography; Enalapril; Female; Follow-Up Studies; Heart Atria; Humans; Male; Tachycardia, Paroxysmal; Time Factors; Treatment Outcome

Obsessive-compulsive disorder (OCD) is briefly characterized, and several of the hypothesized neuroanatomical and neurochemical substrates of this etiologically heterogeneous syndrome are noted. Importantly, alterations in the CNS balance of monoaminergic neurotransmitter systems are probably involved in the pathobiology of OCD. Inasmuch as calcium (Ca) concentration regulates neuronal neurotransmitter release, presynaptic Ca deficiencies can disrupt normal neurotransmission. Supporting this, a case report is presented of a subject with intermittent OCD and comorbid cardiac pathology for whose latter condition a regimen of increasing doses of a Ca channel blocker (CCB) greatly exacerbated the OCD. Upon reducing, then discontinuing the CCB dose, the OCD sympomatology was greatly ameliorated. It is suggested that minimal use of CCBs is indicated for OCD subjects and that, if possible, they be substituted with other drugs. In view of the widespread use of CCBs, this cerebral Ca deficiency hypothesis of OCD etiopathogenesis should be further tested by seeking other OCD subjects, especially from cardiology practices.

Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Brain; Calcium; Calcium Channel Blockers; Enalapril; Humans; Hypertension; Male; Obsessive-Compulsive Disorder; Tachycardia, Paroxysmal; Verapamil