Biomedical subjects
Publications and source records attributed to K M Kessler.
Iatrogenic aortocoronary vein fistula following coronary artery bypass surgery is a rare complication. We describe the first reported case of inadvertent anastomosis of the left internal mammary artery to cardiac vein. The clinical characteristics and consequences as well as the angiographic characteristics of this fistula are described. Precautions that may be taken to prevent this complication are also addressed.
The efficacy of intravenous propranolol for suppression of inducibility of sustained ventricular tachyarrhythmias (VT) was studied in 24 patients who had failed greater than or equal to 1 membrane-active antiarrhythmic drug (mean 2.2 +/- 1.2 drugs/patient). The response to propranolol was compared in 13 patients who had only stable monomorphic VTs inducible at baseline and another 11 patients who had greater than or equal to 1 episode of electrically unstable VTs (polymorphic VT, ventricular flutter or ventricular fibrillation) at baseline. Seven patients (29%) became noninducible (responders) and 17 patients (71%) remained inducible to sustained VT (nonresponders) after propranolol. The basal heart rate was faster in responders than in nonresponders (101 +/- 14 vs 86 +/- 11 beats/min, p less than 0.01). The magnitude of heart rate reduction was also greater after propranolol in responders (from 101 +/- 14 to 80 +/- 9 beats/min, p less than 0.001) than in nonresponders (from 86 +/- 11 to 74 +/- 9 beats/min, p less than 0.01) (p less than 0.05 between the groups), despite equal plasma propranolol concentrations (84 +/- 50 vs 88 +/- 43 ng/ml, difference not significant). Seven of 11 patients (64%) who had greater than or equal to 1 episode of unstable VTs inducible at baseline responded to intravenous propranolol, whereas none of the patients with only stable monomorphic VTs became noninducible after beta blockade (p less than 0.001). Responders had shorter cycle length of inducible VTs than nonresponders (225 +/- 38 vs 302 +/- 66 ms, p less than 0.001). Thus, intravenous propranolol appears to be efficacious in suppressing fast, electrically unstable VTs, compared to monomorphic VTs with slower rates.
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Changes in sinus node rate were measured as an estimate of reflex control of cardiac autonomic tone during 32 episodes of stable ventricular tachycardia (without loss of consciousness) and 21 episodes of unstable ventricular tachycardia (loss of consciousness requiring electrical cardioversion) in 32 patients without retrograde ventriculoatrial conduction. Sinus node rate was measured before induction of ventricular tachycardia (at 5 s intervals during tachycardia) and 5 s after termination of ventricular tachycardia. It increased from 85 +/- 12 beats/min to a maximum of 109 +/- 25 beats/min during stable ventricular tachycardia (p less than 0.001) and from 82 +/- 15 beats/min to a maximum of 105 +/- 34 beats/min during unstable ventricular tachycardia (p less than 0.001). During unstable ventricular tachycardia, the increase in sinus rate was more abrupt and was followed by a sharp decrease beginning before termination of the tachycardia and resulting in a slower rate after termination (56 +/- 15 beats/min) than before tachycardia (p less than 0.001). Stable ventricular tachycardia resulted in a continuous increase of sinus node rate, which remained higher after termination (102 +/- 15 beats/min) than before tachycardia (p less than 0.001). Autonomic mechanisms responsible for changes in sinus rate were evaluated by reinducing the ventricular tachycardia after beta-adrenergic blockade by propranolol in 10 patients. Intravenous propranolol (mean dose 11 +/- 4 mg) had no effect on the magnitude of increase in sinus rate (+18 +/- 6 beats/min before and +17 +/- 7 beats/min after propranolol).(ABSTRACT TRUNCATED AT 250 WORDS)
New balloon-on-a-wire dilation systems allow crossing of severely stenosed coronary arteries owing to their ultra-low profile. However, these systems do not allow for over-the-wire exchange to a larger balloon catheter or insertion of perfusion catheters, should the vessel close abruptly during dilation. Therefore, if the need for such catheters arises, the vessel must be left unprotected during attempts to recross the lesion. We describe a new technique using a combined balloon-on-a-wire system and an exchangeable guidewire, which permits the crossing and dilation of severely stenosed coronary arteries, while at the same time offering vessel protection and balloon catheter exchange.
Despite advances in the treatment of congestive heart failure (CHF), the mortality rate continues to be high. A large number of the deaths are sudden, presumably due to ventricular arrhythmias. Complex ventricular arrhythmias are recorded in as many as 80% of patients with CHF, with nonsustained ventricular tachycardia occurring in 40%. The latter appears to be an independent predictor of mortality. Chronic structural abnormalities responsible for CHF may be the basis for the capability of a ventricle to support life-threatening arrhythmias, which are triggered by premature ventricular contractions. The pathogenesis of arrhythmias is multifactorial. Electrolyte abnormalities, ischemia, catecholamines, inotropic and antiarrhythmic drugs may worsen arrhythmias and increase susceptibility of a ventricle to sustained arrhythmias. Beta-adrenergic blockers and angiotensin-converting enzyme inhibitors have a beneficial effect. The role of various drugs in the pathogenesis and treatment of ventricular arrhythmias is discussed. The efficacy of antiarrhythmic therapy targeted to asymptomatic nonsustained ventricular tachycardia, in order to prevent sudden death, is controversial. Pharmacotherapy guided by electrophysiologic testing is the treatment of choice for patients who have manifest sustained ventricular tachycardia, but patients resuscitated from ventricular fibrillation may require automatic implantable cardioverter defibrillator.
We tested the relationship between the frequency of single premature ventricular complexes (PVCs) of specific QRS morphologies and repetitive forms (RF) of greater than or equal to 2 PVCs. Fourteen patients with multiform PVCs and RFs underwent 8-hour, two-channel continuous electrocardiographic monitoring. After a 2-hour baseline, procainamide was administered intravenously at 25 mg/min until PVC suppression or 1000 mg. Multiple regression analysis was used to relate the frequencies of repetitive forms initiated by PVCs of the most frequent QRS morphology (M1) and the second most frequent QRS morphology (M2) to the frequency of M1 and M2 single PVCs. Parallel changes in the frequency of M1 RFs and M1 PVCs occurred in 9 of 14 patients and parallel changes in the frequency of M2 RFs and M2 PVCs occurred in 7 of 14 patients (i.e., the relationships were concordant). In two patients, M1 RFs related to M2 PVC frequency; in three patients, M2 RFs related to M1 PVC frequency (i.e., the relationships were discordant). Thus concordant frequency distributions were present in 16 of 28 (57%) comparisons, while a discordant relationship occurred in only 5 of 28 (18%) comparisons (p less than 0.005). In conclusion, there is frequent concordance in the frequency distribution of single multiform PVCs and of RFs initiated by PVCs of the same QRS morphology during a pharmacologic intervention.(ABSTRACT TRUNCATED AT 250 WORDS)
Pharmacodynamic and pharmacokinetic aspects pertinent to the potential clinical application of unbound quinidine levels were studied. Following heparin administration during electrophysiologic testing in 10 patients receiving quinidine, there were significant increases in the mean (+/- SD) right ventricular effective refractory period (266 +/- 24 versus 279 +/- 23; p less than 0.025), free fatty acid concentration (515 +/- 213 versus 1071 +/- 359 mmol/L; p less than 0.001), and unbound quinidine concentration (0.3 +/- 0.1 to 0.6 +/- 0.1 microgram/ml; p less than 0.001) but no changes in heart rate, corrected QT interval, or total plasma quinidine concentration. Ten control patients showed no change in the right ventricular effective refractory period following heparin administration. These findings were consistent with a heparin-induced increase in unbound drug concentration and activity that was limited to the vascular compartment. Eleven patients studied on day 3 (+/- 1) and day 10 (+/- 3) during an acute myocardial infarction showed a significant decrease in unbound quinidine fraction (12 +/- 4% versus 9 +/- 4%; p less than 0.02) accompanied by a decrease, rather than the predicted increase, in half-life (7.1 +/- 2.7 versus 6.3 +/- 2.1 hours; p less than 0.02). Volumes of distribution remained stable while the mean quinidine clearance tended to increase. Half-life correlated with albumin changes (r = -0.71; p less than 0.02). Apparently, improvement in clinical status (assumed) and drug clearance (measured) negated the direct effects of the decrease in unbound quinidine fraction. Although unbound drug concentrations should correlate best with drug dynamic and kinetic information, full knowledge of the clinical context of such measurements is needed for appropriate interpretation.
This study was undertaken to better characterize the role of multiform premature ventricular complexes in the classification of ventricular arrhythmias based on form and frequency. Twenty inpatients with organic heart disease and multiform ventricular complexes underwent continuous electrocardiographic monitoring with full disclosure analysis of the number and morphology of single premature ventricular complexes, of repetitive forms of greater than or equal to 2 premature ventricular complexes, and of the variability of coupling intervals (greater than or equal to 40 msec). Multiform premature ventricular complexes were of 3 +/- 1.4 (mean +/- S.D.) different QRS morphologies. Nineteen patients (95%) had repetitive forms of greater than or equal to 2 premature ventricular complexes; 18 patients (90%) showed variable coupling (125 +/- 29 msec). Repetitive forms or variable coupling were present in each (100%) of the 20 patients studied. These data suggest that multiform premature ventricular complexes may be a transitional arrhythmia, since repetitive forms almost always coexist. Variability in coupling, rather than just form and frequency, may be an electrocardiographic characteristic linking single and repetitive forms.
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The use of membrane-active antiarrhythmic agents may be complicated by aggravation of existing arrhythmias or development of new drug-induced arrhythmias. Four patients, referred because of out-of-hospital cardiac arrest or symptomatic sustained ventricular tachycardia, were receiving class IC antiarrhythmic agents in an attempt to prevent inducibility of sustained ventricular tachycardia. New or worsening spontaneous arrhythmias developed while they were on flecainide acetate (n = 3) or encainide hydrochloride (n = 1) therapy. Spontaneous runs of rapid nonsustained and sustained ventricular tachycardia developed in two. Increased frequency of premature ventricular contractions and repetitive forms of ventricular ectopic activity developed in one, despite the fact that inducibility of sustained ventricular tachycardia had been prevented. Salvos and nonsustained ventricular tachycardia developed in the fourth patient. Propranolol had failed to prevent inducibility of sustained ventricular tachycardia during previous programmed stimulation studies in three of the four patients, but it reproducibly suppressed drug-induced arrhythmias that appeared only after administration of the IC agents in each patient. Suppression of the proarrhythmic effects by beta-adrenergic blockade suggests a possible interaction of these drugs with autonomic function in the genesis of the observed proarrhythmic effects. Direct pharmacologic control of proarrhythmic drug effects has not previously been reported.
The effect of an infusion of intravenous procainamide on the frequency of ventricular premature complexes (VCPs) of differing QRS morphologies was studied in 20 patients with multiform ectopic activity. In 17 of 20 patients, there was differential suppression of single VPCs with different QRS morphologies. VPCs of the most frequent QRS morphology and the second most frequent QRS morphology were compared with respect to the procainamide level at the escape of VPCs from 85% suppression and the duration of suppression measured from the onset of the procainamide infusion. In 8 patients, VPCs of the most frequent QRS morphology remained suppressed at lower procainamide concentrations and for longer times than did VPCs of the second most frequent QRS morphology (escape procainamide concentration = 2.8 +/- 1.7 versus 5.4 +/- 2.3 micrograms/ml, p less than 0.025; time to escape 244 +/- 138 versus 98 +/- 114 min; p less than 0.05). In 9 other patients, VPCs of the second most frequent QRS morphology remained suppressed at lower procainamide concentrations and for longer times than did VPCs of the most frequent QRS morphology (escape procainamide concentration 2.9 +/- 1.4 versus 8.3 +/- 6.3 micrograms/ml, p less than 0.025; time to escape 317 +/- 114 versus 63 +/- 80 min; p less than 0.001). Thus, in individual patients there are specific patterns of suppression of VPCs of different QRS morphologies which are independent of the frequency of each morphology. There is apparently a differential pharmacologic effect of procainamide on the foci or pathways responsible for the different QRS morphologies of multiform VPCs.
Clinical, angiographic, and pathologic data support the contention that atherosclerosis, platelet aggregation, and coronary vasomotility work in unison to cause coronary thrombosis, which in turn leads to myocardial infarction. A patient is described in whom, 2 months after an acute myocardial infarction, inducible coronary artery spasm and a nonocclusive thrombus were angiographically demonstrated at the site of a minimal atherosclerotic narrowing in the infarction-related vessel. This report, to the best of our knowledge, is the first time that these three pathophysiologic mechanisms have been shown, in vivo, to be occurring concomitantly in an infarct-related vessel. Documentation of the unified occurrence of these phenomena support the current concept of the pathophysiology of myocardial infarction.
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