This study prospectively examined the role of cognitive behavioral therapy (CBT) in (1) alleviating psychological and somatic distress, and (2) lowering arrhythmic events requiring shocks. Forty-nine of 61 consecutive patients were randomized into therapy (CBT, n = 25) or no therapy (NT, n = 24) and completed a battery of self-report questionnaires at baseline and at 9-month follow-up. CBT was administered at preimplant, predischarge, and at seven routine follow-up visits. Patients were 65 +/- 10 years old, 65% were men, and 92% Caucasian. Eighteen (72%) CBT patients and 18 (75%) NT patients were retained at follow-up. Compared to CBT patients, NT patients reported higher levels of depression (P = 0.046), more anxiety (P = 0.013), more psychological distress (P = 0.015), poorer overall adjustment (P = 0.009), and poorer sexual functioning (P = 0.003). Mean number of shocks did not differ between the CBT and NT groups (2.85 vs 2.30, respectively); however, more patients in the CBT group (61%) than the NT group (33%) received shocks (P = 0.070). At follow-up, a subgroup analysis revealed that the significant differences observed between the CBT and NT groups were attributable to the patients who received shocks in both groups. In conclusion, CBT was associated with decreased depression, decreased anxiety, and increased adjustment for ICD recipients, particularly among those patients receiving shocks. CBT can be administered effectively at routine follow-up visits or transtelephonically with little added inconvenience to the ICD recipient.
Cyclosporin-A (CsA) inhibits the in vitro bone-resorbing effects of cytokines. We investigated the in vivo effects of CsA on rat bone mineral metabolism. Three groups of male Sprague-Dawley rats were administered vehicle or low dose (7.5 mg/kg) or high dose (15 mg/kg) CsA for 14 and 28 days. Ionized calcium, PTH, serum bone Gla protein, blood urea nitrogen, creatinine, magnesium, and 1,25-dihydroxyvitamin D were determined serially. No significant changes in calciotropic hormones or renal function were noted. Significant bone resorption and trabecular bone loss occurred in the high dose group by day 14 and in both groups by day 28. Bone Gla protein was significantly increased within 2 weeks in both dosage groups (P less than 0.005), reflecting increased bone remodeling. CsA in vivo resulted in an unexpected and significant increase in bone remodeling, with striking bone loss. These effects are dependent on the duration and dose of CsA and appear to be mediated at a local level.
Isthmus conduction block is associated with flutter ablation success. Conduction slowing or intermittent block, or both, in the isthmus can occur before achieving persistent block. Recovery of conduction after achieving block is common. Follow-up has revealed a low rate of flutter recurrence after achieving isthmus conduction block, whether the block was achieved in conjunction with termination of flutter.
The in vivo administration of cyclosporin A (CsA) has been associated with significant bone loss and increased bone remodeling. To observe whether these changes are reversible, we have investigated the consequences of the administration and withdrawal of CsA immunotherapy on bone mineral metabolism. Three groups of Sprague-Dawley rats were studied for 28 days. Group A received vehicle, and group B received CsA (15 mg/kg BW) for 28 days, while group C received CsA (15 mg/kg BW) for 14 days and then vehicle from days 15-28 by daily gavage. Serum ionized calcium (Ca2+), PTH, bone gla protein, blood urea nitrogen, creatinine, magnesium, phosphorus, and 1.25-dihydroxyvitamin D were measured weekly. Bone histomorphometry was analyzed on days 14 and 28 in groups A and B and on day 28 in group C. CsA administration resulted in reversible hypomagnesemia and mild transient elevation in circulating 1,25-dihydroxyvitamin D levels with no change in Ca2+, PTH, blood urea nitrogen, or phosphorus. Serum bone gla protein levels were significantly increased (P less than 0.002) during CsA therapy, but tended to return to control values after CsA withdrawal. Enhanced bone remodeling and significant trabecular bone loss accompanied CsA administration. Withdrawal of CsA resulted in all of the histomorphometric parameters, except for bone volume, returning to control values within 2 weeks. Incomplete restoration of bone volume occurred 5 weeks after CsA withdrawal. This limited restoration of bone volume despite CsA withdrawal may have important clinical implications.
There has been progressive development in ambulatory external electrocardiogram (AECG) monitoring technology. AECG monitors initially consisted of 24- to 48-h Holter monitors and patient-activated event and loop recorders. More recently, several ambulatory cardiovascular telemetry monitors and a patch-type 7- to 14-day Holter monitor have been introduced. These monitoring systems are reviewed along with their utility and limitations, with particular emphasis on their role in the diagnosis and evaluation of patients with atrial fibrillation (AF). AECG monitoring is necessary when asymptomatic AF is suspected (as in patients presenting with cryptogenic stroke) or when an ECG diagnosis of unexplained arrhythmic symptoms is warranted. In addition, AECG plays an important role in patients with known AF to guide ventricular rate control and anticoagulation therapy, and assess the efficacy of antiarrhythmic drug therapy and/or ablation procedures. Finally, we outline areas of uncertainty and provide recommendations for use of available AECG monitors in clinical practice.
Catheter ablative therapy for the arrhythmias attempted in the very elderly appears to be effective with low risk. Ablation results appear to be comparable with those noted in younger patients.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.