Influence of aortic impedance on left ventricular function in aortic stenosis.
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Biomedical subjects
Publications and source records attributed to K K Sethi.
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Clinical and electrophysiological features of 20 patients presenting with ventricular tachycardia (VT) of left bundle branch block (LBBB) morphology without evidence of coronary artery disease were studied. The mean age of the patients was 35.2 +/- 12 (range 15-57 years). The rate of VT varied between 140-240/min (182 +/- 80). Six (30%) patients experienced giddiness or syncope during palpitations. Structural heart disease was found in 10 (50%) of these patients, which included arrhythmogenic right ventricular dysplasia in five, submitral left ventricular (LV) aneurysm in one, anterolateral LV dyskinesis in one, dilated cardiomyopathy in one, endomyocardial fibrosis in one and nonobstructive hypertrophic cardiomyopathy in one case. Ten patients were free of structural heart disease. Electrophysiological study was done in all patients. VT with same morphology as spontaneous VT was inducible in only 14 patients. Seventeen patients were treated medically with total or partial amelioration of symptoms. In three patients, two with arrhythmogenic right ventricular dysplasia and one with structurally normal heart, who were unresponsive to drug therapy, the VT focus could be mapped in right ventricular outflow tract and successful electrical ablation was done. Thus in patients who present with VT with LBBB morphology, the heart is often structurally normal but organic disease is not uncommon, and should be carefully searched.
Single-chamber ventricular pacing has been implicated in the development or progression of congestive heart failure in patients with sick sinus syndrome (SSS). To define the exact role of pacing modality in causation of congestive heart failure, quantitative two-dimensional echocardiographic examination was performed in 51 consecutive patients with SSS who received an initial pacemaker from January 1979 to September 1989 and were free of any structural heart disease at the time of implant. Atrial or dual chamber pacemakers were implanted in 21 patients (Group I) and ventricular pacemakers in 30 (Group II). The two groups were matched for age, gender, paced rate, blood pressure and duration of pacing. After a mean follow-up of 64 +/- 34 months, congestive heart failure developed in one patient in group I and 3 in Group II. Patients in group II, had larger left atrium (41 +/- 5 vs 37 +/- 6 mm, p < 0.05) and left ventricular end-diastolic volume (64 +/- 18 vs 54 +/- 12 ml/m2, p < 0.01) but similar left ventricular end-systolic volume (27 +/- 12 vs 24 +/- 9 ml/m2, p = NS), ejection fraction (59 +/- 10 vs 57 +/- 8%, p = NS), left ventricular mass (84.8 +/- 31 vs 85.6 +/- 29.2 gm/m2, p = NS), meridian end-systolic wall stress (48.3 +/- 22.1 vs 49.8 +/- 25 Kdynes/cm2, p = NS) and wall stress/end-systolic volume ratio (1.27 +/- 0.94 vs 1.42 +/- 0.59, p = NS). Pacing mode does not appear to influence left ventricular systolic function in patients with SSS.
The efficacy and electrophysiologic effects of adenosine and verapamil in termination of paroxysmal supraventricular tachycardia (SVT) were compared in 18 patients (age 18-48 years, mean 33 +/- 9 years) with recurrent sustained and inducible SVT. Ten patients had atrioventricular nodal reentrant tachycardia (AVNRT) and 8 had atrioventricular reentrant tachycardia involving a retrograde accessory pathway (cycle length of SVT 280-360 msec; mean 315 +/- 20 msec). Each patient served as his own control. After induction of SVT, adenosine was administered first (6 mg i.v. bolus). If the tachycardia was not terminated, a bolus of 12 mg was given. Ten minutes later, verapamil (5 mg i.v. over 30 sec) was administered after reinduction of SVT. If the tachycardia was not terminated, a 5 mg dose was repeated every 5 minutes upto 20 mg. Adenosine terminated the SVT in 16 cases (6 mg - 7 patients, 12 mg - 9 patients). Verapamil was effective in 11 patients (5 mg - 6 patients, 10 mg - 4 patients, 15 mg - 1 patient, 20 mg - nil). The overall efficacy of adenosine (89%) was significantly greater than that of verapamil (61%; p < 0.05). Adenosine terminated the tachycardia more quickly than verapamil (mean 24 +/- 11 sec versus 142 +/- 40 sec; p < 0.01). Termination of tachycardia by both drugs was related to antegrade block of the atrioventricular node in all patients except one with AVNRT in whom adenosine blocked the retrograde fast pathway. Ventricular premature beats were seen transiently in 5 patients following adenosine. Transient side effects such as flushing, burning and chest pain were frequently observed with adenosine and correlated with the termination of tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)
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Long term performance of 163 atrial leads implanted in 158 patients between July 1981 and June 1993 was evaluated. There were 122 DDD and 36 AAI units, with 125 (77%) polyurethane and 38 (23%) silicone leads. One hundred and nine (67%) unipolar and 54 (33%) bipolar leads were used. Patients were followed in the Pacemaker Clinic for 6 to 124 months (mean 50 +/- 39 months). Five patients were lost to follow up. Transient malfunction was observed in 18 cases (sensing 13, pacing 5) within the first 2 weeks. In 13 cases failure to sense subsided spontaneously and in 4 pacing malfunction could be corrected by reprogramming. Lead dislodgement occurred in 4 patients (2.5%), all within the first week. After the 1st month malfunction was uncommon. Between 1 and 12 months undersensing occurred in 4 (2.5%). In 3 cases it could be corrected by reprogramming. In the first year, reoperation was performed in 5 cases for lead related problems (3 dislodgements, 2 insulation failures). Beyond 12 months complications were as follows: failure to sense-8 (5%), failure to pace-3 (2%), insulation break -1 (0.6%). Majority of these problems could be managed by reprogramming. Reoperation was performed in 1 case with insulation break. The pacing mode had to be changed in 5 (3%) patients with dual chamber units who had loss of P wave sensing. During follow-up 98%, 98%, 96%, 95% and 83% of the leads were working satisfactorily at 1,2,3,4 and 9 years respectively. Thus atrial leads have excellent long term performance and an acceptable rate of late malfunction.
The efficacy and safety of amlodipine was evaluated in 20 patients with stable exertional angina. Patients with > or = 3 anginal attacks per week in the placebo run-in phase were admitted into a 4 weeks active treatment phase. Amlodipine was administered at a starting dose of 5 mg once daily at bed time, which could be adjusted after 2 weeks to 10 mg once daily if the patient continued to have even a single anginal attack/week. Four weeks of treatment with amlodipine produced a significant (p < 0.05) reduction from baseline in both the mean (+/- SE) number of anginal attacks/week (from 13.3 +/- 1.5 to 1.6 +/- 0.5) and the mean (+/- SE) number of isosorbide dinitrate tablets consumed per week (12.1 +/- 1.5 to 2.6 +/- 0.8). Eighty three percent of patients required an increase in dose to 10 mg daily. No significant change in heart rate, blood pressure, ECG and laboratory results were observed. One patient was withdrawn because of deteriorating angina and sinus tachycardia secondary to beta blocker withdrawal. Worsening of ankle odema was reported in 2 (10%) patients, which was tolerated and disappeared on completing therapy. Thus amlodipine is safe and effective when used as monotherapy in the treatment of chronic stable angina.
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The efficacy and safety of amlodipine was evaluated in 20 patients of mild to moderate hypertension in a single blind, placebo controlled, noncomparative study. Patients with a baseline diastolic blood pressure of > 90 and < 115 mmHg while on placebo were admitted to a 4 week active treatment phase. Amlodipine produced a significant (p < 0.05) reduction in mean systolic (177 mmHg to 145 mmHg) and diastolic blood pressure (106 mmHg to 84 mmHg) after 4 weeks treatment in all patients. 95% of the patients had their diastolic blood pressure reduced to < or = 90 mmHg by the end of the study period. There was no significant change in heart rate or in the laboratory parameters with amlodipine therapy. Seven patients reported mild to moderate adverse events which did not require discontinuation of therapy. This combination of efficacy and tolerability, together with convenience of once daily dosing, should ensure the usefulness of amlodipine in the treatment of hypertension.
Thirteen patients with ruptured sinus of Valsalva aneurysm have been operated over a 3-1/2 year period. Right coronary sinus was predominantly involved and right ventricle was the most common site of rupture. Early surgery was performed in all cases. Both aorta and chamber of entry were explored for effective repair. Main repair was always done in the chamber of rupture either with a patch or interrupted pledgeted sutures followed by assessment at either end. Subannular ventricular septal defects in three cases were closed with a common patch with additional fixation in the middle at the aortic annulus to prevent aortic leak into the left ventricle. Three patients needed aortic valve replacement for gross aortic incompetence. Postoperative echocardiographic study revealed uniformly excellent results with good aortic valve or prosthetic function. One patient developed fatal pulmonary embolism two weeks following surgery. All other surviving patients are doing well and are in NYHA class I. We recommend dual exposure and repair technique for the repair of ruptured sinus of Valsalva aneurysms for optimal results.
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Two patients with recurrent episodes of symptomatic, sustained monomorphic ventricular tachycardia (VT) resistant to medical therapy underwent catheter ablation for the relief of VT. One patient had arrhythmogenic right ventricular dysplasia while the other had no structural heart disease. The VT had left bundle branch block morphology with normal axis in both the patients. The cycle length during VT was 260 msec and 270 msec respectively. Site for ablation was guided by pacemapping and the target site was identified in the right ventricular outflow tract in both the patients. Two cathodal shocks of 200 J in the first patient and one shock of 200 J in the second patient resulted in abolition of the arrhythmia. At repeat electrophysiologic testing at 7 days in the first patient and at 8 months in the second, VT was not inducible despite three extrastimuli from two right ventricular sites. Over a follow up of 24 and 26 months respectively, there has been no recurrence without any antiarrhythmic therapy. There were no acute or long term complications. In conclusion, catheter ablation offers a cure in patients with right ventricular tachycardia resistant to antiarrhythmic drugs.
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