Coronary artery revascularization in patients with sustained ventricular arrhythmias in the chronic phase of a myocardial infarction.
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Biomedical subjects
Publications and source records attributed to P Khairy.
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Compensatory changes in ion transport mechanisms occur in response to a variety of cardiac disease processes. Recent work has demonstrated that these adaptive responses can produce the arrhythmogenic substrate for a variety of important cardiac rhythm disorders. Two important paradigms are atrial tachycardia-induced remodeling and ionic remodeling caused by congestive heart failure. Atrial tachycardia promotes cellular Ca(2)+ loading and downregulates a variety of ion channels, particularly L-type Ca(2)+ channels, thereby promoting the occurrence and maintenance of atrial fibrillation. Congestive heart failure alters the expression and function of a variety of membrane transport processes, including several K(+)-channels and key Ca(2)+-transport systems, favoring the occurrence of arrhythmogenic afterdepolarizations. An improved understanding of the mechanisms and consequences of arrhythmogenic ionic remodeling promises to lead to novel and improved therapeutic approaches.
Modern pacemakers offer many programming options regarding the AV interval including the ability to vary AV intervals depending on whether atrial activity is paced or spontaneous and to shorten AV intervals with increasing rates. To determine if optimization of these features improves exercise tolerance, 14 patients with intact sinus node function and AV block treated with dual chamber pacemakers were enrolled in a randomized double-blind crossover trial. Doppler echocardiographic measurements of cardiac index and mitral flow were assessed over a range of programmable AV intervals at rest to determine each patient's optimal AV interval. Eleven patients completed serial graded exercise tests with spiroergometry after randomly programming the AV interval three ways in a crossover manner: fixed AV interval = 150 ms without rate adaptation (150/Fixed), fixed AVinterval = 150 ms with rate adaptation (150/R), or optimized AV interval with rate adaptive AV interval shortening (optimized/R). Exercise capacity was determined by maximum oxygen uptake. Ten men and four women, age 64 +/- 8 years, were enrolled. At rest, optimization of the AVintervalimproved the cardiac index by 21% (P < 0.001) and mitral flow by 13.4% (P < 0.001) when compared to least-favorable AV intervals. During exercise, no differences in maximum heart rates were noted. Maximum oxygen uptake was increased in both groups with rate adaptive AVinterval shortening when compared tofixed AVinterval without rate adaptation: 13.9% (adjusted P < 0.04) and 14.6% (adjusted P < 0.02) in optimized/R and 150/R, respectively. No differences were noted between optimized/R and 150/R. In conclusion, rate adaptive AV interval shortening improved exercise tolerance independent of changes in heart rate. However, optimization of the AV interval with Doppler echocardiography at rest did not further improve exercise capacity.
INTRODUCTION: Recent animal studies demonstrated the feasibility and safety of applying percutaneous catheter cryoablation technology for ablation of arrhythmogenic sites. The studies also showed that reversible "ice mapping" can be performed before creating permanent lesions. We investigated the feasibility and safety of applying this new technology in man. METHODS AND RESULTS: Cryoablation of the AV node (AVN) using a 9-French quadripolar catheter with a 4-mm electrode tip was attempted in 12 patients (mean age 67.8 +/- 11.4 years) with refractory atrial fibrillation. Whereas technical issues prevented adequate tissue contact in two patients, complete AVN block was obtained in the remaining 10 patients after 4.8 +/- 1.9 cryoapplications lasting 5.5 +/- 0.2 minutes resulting in temperatures of -58.1 degrees +/- 5.4 degrees C. In all patients with sinus rhythm at the time of the procedure, cryomapping at warmer temperatures induced reversible AVN block and allowed confirmation of a successful site before definitive ablation. Intracardiac echocardiography was performed in three patients and allowed visualization of the cryocatheter-endocardial contact and cryolesion formation. No major procedural complications were reported. After 6 months of follow-up, 8 of 10 initially successful patients remained in complete block; 1 had partial recovery of AVN conduction manifested by atrial fibrillation with a slow ventricular response, and 1 fully recovered AVN conduction. CONCLUSION: (1) Catheter cryoablation of the AVN can be performed safely in man. (2) Reversible cryomapping is feasible and may offer an advantage over radiofrequency ablation. (3) Cryocatheter-endocardial contact and cryolesion growth can be monitored with intracardiac echocardiography.
A 64-year-old woman with mild acute pancreatitis presented with epigastric pain, nausea and vomiting while undergoing hemodialysis for chronic renal insufficiency. Serial electrocardiograms revealed new onset ST segment elevations in leads V2 to V4 mimicking an anterior myocardial infarction, followed by diffusely inverted deep T waves. No cardiac pathology was demonstrated by echocardiography or coronary angiography. A review of the literature and possible pathophysiological mechanisms of electrocardiographic changes in acute pancreatitis, such as metabolic abnormalities, hemodynamic instability, vasopressors, pericarditis, myocarditis, a cardiobiliary reflex, exacerbation of underlying cardiac pathology, coagulopathy and coronary vasospasm, are discussed.
A 50-year-old man with Whipple's disease was found to have a positive Kussmaul's sign, prominent jugular V waves and a pansystolic murmur. Echocardiography revealed severe tricuspid regurgitation and moderate aortic and mitral regurgitation. Thickening of the noncoronary aortic cusp, calcification of the mitral annulus and a possible calcified density embedded in the left ventricular free wall were also noted. A review of the literature demonstrates high prevalence of cardiac manifestations in patients with Whipple's disease. Constrictive pericarditis, valvular deformity, myocarditis, coronary arteritis, congestive heart failure and sudden death have been documented. No clear relationship between the extent of cardiac involvement and the severity of the systemic disease has been shown, and the efficacy of antibiotic treatment for cardiac lesions remains to be demonstrated.