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Biomedical subjects

J J Kane

Publications and source records attributed to J J Kane.

At least 37 records · Page 2Linked to original sources

The relationship of paroxysmal ventricular tachycardia complicating the acute phase and ventricular arrhythmia during the late hospital phase of myocardial infarction to long-term survival.

The long-term prognosis of paroxysmal ventricular tachycardia (PVT) complicating acute myocardial infarction remains unevaluated. Significant ventricular arrhythmia in the patient after infarction is said to carry a poor prognosis with regard to survival. To evaluate these two important aspects of myocardial infarction in man, 56 patients with documented myocardial infarction had Holter monitoring performed during the initial 24 hours and prior to hospital discharge. In 38 of the 45 survivors, Holter monitoring was repeated an average of 19 months after infarction. There were eight cardiac deaths during follow-up. Data analysis revealed that of 18 patients with PVT during the acute phase, one died during follow-up and 17 survived long-term. Even though the incidence of complex PVCs prior to hospital discharge and at long-term follow-up was higher in patients with PVT during the acute phase than in those without PVT, survival appeared unaffected. Thus, PVT during the acute phase of myocardial infarction and complex PVCs at the time of hospital discharge are not incompatible with long-term survival.

Acute Disease↗

Effect of digitalis on human ventricular refactoriness.

In order to evaluate the effect of digitalis on the effective refractory period of the human ventricle, 14 patients were studied with atrial or ventricular pacing and with the introduction of ventricular extra-stimuli. The ventricular effective refractory period (VERP) was recorded before and after 1.0 to 1.25 mg ouabain given intravenously and the results compared with similar changes in the Q-T interval. During atrial pacing (eight patients) at rates of 70 to 110 beats per minute, ouabain reduced the mean ventricular effective refractory period from 290 +/- 13 ms to 260 +/- 16 ms (P less than 0.01) and the mean Q-T interval was reduced from 372 +/- 18 ms to 359 +/- 19 ms (P less than 0.01); the mean VERP/Q-T ratio was 0.79 +/- 0.04 before ouabain and 0.73 +/- 0.04 after ouabain (P less than 0.01). Utilising ventricular drive pacing (six patients) the mean ventricular effective refractory period was reduced from 245 +/- 16 ms to 226 +/- 13 ms (P less than 0.01) and the mean Q-T interval reduced from 382 +/- 18 ms to 360 +/- 29 ms (P less than 0.01). There was no significant change in the mean VERP/Q-T ratio (0.63 +/- 0.04 before vs 0.63 +/- 0.04 after ouabain). The results demonstrate that clinically effective doses of ouabain produce a significant reduction of the effective refractory period of the human ventricle. This change is accompanied by a reduction in the VERP/Q-T ratio during atrial pacing.

Adult↗

Ventricular arrhythmias in chronic stable angina pectoris with surgical or medical treatment.

Since both propranolol therapy and saphenous-vein bypass surgery have become accepted treatments for patients with symptomatic coronary-artery disease, it is important to determine if either influences the prevalence of ventricular arrhythmias in these patients. Six-hour dynamic electrocardiography was done on 130 patients with chronic stable angina pectoris at least 1 year after being randomized to surgical or medical therapy. All surgical patients had saphenous-vein grafting; 90% of the medical patients received propranolol. Data analysis showed that even though the overall prevalence of premature ventricular contractions was no different in medical and surgical patients, the prevalence of complex premature ventricular contractions was significantly higher in surgically treated patients not receiving propranolol than in propranolol-treated medical patients (p less than 0.05). However, the survival rate was no different in either group, and the quality of life in the surgical patients remained superior.

Adult↗

Effects of adenine nucleotide translocase inhibitors on dinitrophenol-induced Ca2+ efflux from pig heart mitochondria.

Bongkrekic acid and atractyloside, inhibitors of adenine nucleotide translocase, do not inhibit Ca2+ uptake and H+ production by pig heart mitochondria. However, bongkrekic acid, but not atractyloside, inhibits dinitrophenol-induced Ca2+ efflux and H+ uptake. Conversely, ruthenium red blocks Ca2+ uptake and H+ production but does not prevent dinitrophenol-induced Ca2+ efflux and H+ uptake by mitochondria. These results suggest that mitochondrial Ca2+ uptake and release exist as two independent pathways. The efflux of Ca2+ from mitochondria is mediated by a bongkrekic acid sensitive component which is apparently not identical to the ruthenium red sensitive Ca2+ uptake carrier.

Adenosine Diphosphate↗

Dual effects of concealed A-V nodal conduction in man.

An interpolated premature ventricular contraction (PVC) may produce either complete block of the next sinus impulse or depression of A-V nodal conduction with a prolonged A-H interval. When a PVC results in partial depression of a A-V nodal conduction, the effect on subsequent premature atrial stimuli is unknown. The authors have recently observed three patients in which the effect of a premature ventricular stimulus with interpolation on the functional refractory period of the A-V node could be measured. In case one an interpolated PVC sufficient to prolong the A-H interval from 80 to 120 msec was followed by programmed premature atrial stimuli which resulted in no additional A-V nodal delay, and the apparent functional refractory period of the A-V node was reduced from 420 to 330 msec when compared with the atrial extrastimulus technique. In case two a programmed ventricular extrastimulus prolonged the A-H interval in the following sinus beat from 120 to 240 msec; atrial extrastimuli then resulted in only minimal increments in A-V nodal delay and the apparent functional refractory period of the A-V node was reduced from 590 msec. A ventricular extrastimulus in case three increased the resting A-H interval from 60 to 115 msec; conduction of atrial extrastimuli then resulted in a reduction in the functional refractory period of the A-V node from 465 to 400 msec. In each case an interpolated premature ventricular stimulus produced (1) depression of A-V nodal conduction in the ensuing sinus beat A1 and (2) relative facilitation of A-V nodal conduction of a subsequent premature atrial stimulus (A2). The functional refractory period of the A-V node was reduced when compared with the atrial extrastimulus technique alone.

Atrioventricular Node↗

Experimental production of manifest and concealed ventricular rhythms in man.

Analysis of clinical ventricular ectopy has provided deductive evidence for the existence of concealed ventricular rhythms. Studies in the experimental animal have demonstrated that when ventricular extrastimuli are applied near the ventricular effective refractory period of consecutive sinus beats, extrastimuli may not be conducted after sinus beats immediately following the post-estrasystolic pause. This sequence may be due to a prolongation of the effective refractory period of ventricular muscle produced by the increased cycle length resulting from the post-extrasystolic pause. The purpose of this study was to extend these observations to the human ventricle in an attempt to produce concealed ventricular rhythms by programmed ventricular extrastimuli. Twelve patients with normal PR intervals and QRS complexes with a mean age of 49 years were studied with ventricular extra-stimuli at programmed intervals following normally conducted sinus impulses. Premature ventricular impulses were introduced after every sinus beat at intervals 10 to 120 msec outside the effective refractory period. In eleven patients without ventricular interpolation, stimuli applied within 40 msec of the effective refractory period produced from one to three concealed (non-conducted) ventricular stimuli following the post-extrasystolic pause; stimuli applied greater than 40 msec outside the effective refractory period at identical current levels produced manifested bigeminy in all cases. In one patient with interpolated premature ventricular beats without a compensatory pause, programmed ventricular extrastimuli produced manifest bigeminy at all coupling intervals. This study demonstrates the experimental production of concealed and manifest ventricular rhythms in man and confirms the importance of the relationship between the ventricular effective refractory period, the timing of the premature ventricular impulse, and the occurence of a compensatory pause.

Electric Stimulation↗

Detecting ventricular arrhythmia after myocardial infarction: comparison of Hoiter monitoring and treadmill exercise.

The effectiveness of Holter monitoring is compared to modified treadmill exercise for detecting ventricular arrhythmia in 54 patients during the third week after a documented myocardial infarction. Treatment with digoxin and antiarrhythmic agents had been discontinued for 48 hours. Whereas 76% of the patients had no PVCs during treadmill exercise, only 7% were free of PVCs during Holter monitoring. Complex PVCs occurred in 37% of the subjects during Holter monitoring and in 4% of the subjects during treadmill stress. Although Holter monitoring was significantly more reliable in detecting ventricular arrhythmia, assessment of exercise tolerance and angina status during modified treadmill stress makes both technics desirable in carefully selected patients awaiting discharge from the hospital after myocardial infarction.

Adult↗

Digitalis in pulmonary heart disease (cor pulmonale).

The use of digitalis in pulmonary heart disease has been a topic of great interest for a number of years. The physician's decision to use or not to use digitalis in pulmonary disease has often been an emotional rather than a reasoned one. The diagnostic difficulties from a clinical point of view in separation of pulmonary from cardiac symptoms and findings have also been confusing. The fact that small doses of digitalis may have an inotropic effect on the cardiac muscle has been a difficult concept for many physicians to adopt. On the other hand, the larger doses of digitalis that are often necessary to control the ventricular response in supraventricular arrhythmias sometimes gives rise to confusion. We shall attempt to review the subject in detail and examine indications, contraindications, toxicity, dosage, assessment of benefit, and role of digitalis serum levels in patient management.

Arrhythmias, Cardiac↗

Pharmacokinetics of digoxin.

The pharmacokinetics of digoxin, the most frequently used digitalis preparation, are reviewed. The dominate serum turnover time is about 34 hours, and is not affected by the route of administration. Excretion is largely as unchanged digoxin in the urine and this excretion is compromised in renal failure. Serum levels of digoxin (determined by radioimmunoassay) are generally available and are useful clinically in assessment of both toxicity and the state of underdigitalization, even though significant overlap exists. Special problems are presented in patients with myocardial infarction, pulmonary heart disease, and thyroid disease.

Acute Kidney Injury↗

The relation of sinus rate to the frequency of paroxysmal ventricular tachycardia during acute myocardial infarction in man.

Continuous tape recordings of cardiac rhythm were made in 51 male patients with acute myocardial infarction within 24 hours of their infarction. These tracings were analyzed for the incidence of paroxysmal ventricular tachycardia (PVT) and the sinus rate immediately preceding each episode of PVT. In 26 patients, 112 episodes of PVT at a rate greater than 100 beats/min were documented. Although 67 per cent of the episodes of PVT were preceded by sinus rates between 60 and 100 beats/min, 15 per cent occurred at sinus rates below 60 beats/min and 18 per cent occurred at sinus rates above 100 beats/min. The data remained essentially unchanged regardless of whether ventricular tachycardia was defined at rates in excess of 100, 120 or 140 beats/min. The results of this study show that during the early phases of acute myocardial infarction in man, PVT was most common during sinus rates generally thought to be within the normal range (60 to 100 beats/min). A lower, but close to equal incidence of PVT was observed during sinus bradycardia and sinus tachycardia.

Adult↗

Comparison of the effects of atrial and ventricular stimulation on sinus node function in man.

Although sinus node function has been evaluated during premature atrial stimulation, no study of retrograde ventriculoatrial sinus node activation following premature ventricular stimuli has been reported. The purpose of this study was to investigate the production of compensatory and noncompensatory pauses by premature ventricular contractions through a comparison of the effects of atrial and ventricular stimulation on sinus node function. Eleven patients in sinus rhythm were studied with programmed introduction of premature atrial and ventricular stimuli outside the ventricular vulnerable period. The onset of sinus node reset, duration of return sinus cycle (A2-A3) during reset, and estimated sinoatrial conduction times were recorded. Sinus node function during premature ventricular stimulation was approximated by utilizing the interval between the last sinus beat and onset of retrograde atrial depolarization (A1-A2 interval). The return cycle length (A2-A3) during sinus reset compared at equal A1-A2 intervals was significantly less with ventriculoatrial conduction (1,145 +/- 52 msec. atrial vs. 1,076 +/- 52 msec ventriculoatrial; P less than 0.01 by paired t test) and the estimated sinoatrial conduction time was significantly less with ventriculoatrial conduction (71 +/- 7 msec. atrial vs. 25 +/- 7 msec. ventriculoatrial; P less than 0.01 by paired t test). Ventriculoatrial sinus reset occurred later in the sinus cycle than atrial reset in three of seven patients with sinus reset produced by both atrial and ventricular prematures. This study shows that the effects of ventriculoatrial conduction on sinus node function are significantly different from those of atrial stimulation alone. The return sinus cycle length during reset and estimated sinoatrial conduction time are significantly reduced with ventriculoatrial conduction. Although the zones of sinus reset with atrial and ventricular stimulation are approximately equal, ventriculoatrial depolarization may produce sinus reset later in the sinus cycle in some cases.

Adult↗

Atrioventricular conduction patterns in patients with paroxysmal supraventricular tachycardia.

Atrioventricular conduction patterns suggestive of dual A-V nodal pathways have been reported in patients with and without a history of paroxysmal A-V nodal re-entrant tachycardia (PSVT). The purpose of this study was to determine whether significant association exists between this conduction pattern and the occurrence of PSVT in man. The pattern of A-V conduction was evaluated at similar pacing rates in 13 patients with documented PSVT and 135 patients with PSVT. Patients without PSVT were divided into groups with normal PR intervals (106 patients), PR intervals of 120 msec. or less (12 patients), and PR intervals of 200 msec. or greater (17 patients). Evidence of dual A-V nodal pathways was found in seven of 13 patients with PSVT and nine of 135 patients without PSVT, including eight of 106 patients with normal PR intervals, none of 12 patients with short PR intervals, and one of 17 patients with PR intervals of 200 msec. or greater. The incidence of dual A-V nodal pathways was significantly greater (P less than 0.01) in patients with PSVT when compared with all other groups. In two of four patients with PSVT, propranolol was found to unmask evidence of dual pathways; no evidence of dual pathways was produced by propranolol in 23 patients without PSVT. The data show that the pattern of dual A-V nodal pathways is common only in patients with PSVT and is significantly less frequent in patients without PSVT regardless of the presence of short or long PR intervals. The results of this study establish a strong association between this conduction pattern and the occurrence of PSVT in man.

Adult↗

Improved sinus node sensing after atropine.

Although atropine is known to increase sinus rate through its vagolytic effect, the effects of atropine on sinus node sensing are unknown. The purpose of this study was to investigate alterations in sinus node sensing produced by atropine. Measurement of the zone of sinus node reset and sinoatrial conduction time was performed in 10 patients by programmed premature atrial stimulation. The zone of sinus node reset was determined as the transition point where premature atrial stimuli were followed by a less than compensatory pause. Sinoatrial conduction time was calculated from sinus node return cycles in the area where sinus node reset occurred. Atropine administration produced a significant increase in the percentage of the sinus cycle length at which premature atrial contractions penetrated and reset the sinus node. Sinus node reset occurred at a mean percentage of the sinus cycle of 71 +/- 8 per cent before atropine and 83 +/- 5 per cent after atropine (P less 0.01). The sinoatrial conduction time was significantly reduced from 109 +/- 29 to 62 +/- 23 msec. (P less than 0.01) from atropine as sinus cycle length was reduced from 909 +/- 118 to 642 +/- 75 msec. after atropine. Sinus node echoes were observed in two patients. In one patient atropine abolished the appearance of sinus node echoes. In the second patient atropine reduced the coupling interval necessary to produce sinus node echoes but appeared to facilitate sinus node re-entry by the appearance of an additional sinus node echo and a reduction in the echo cycle length. This study demonstrates that atropine produces significant improvement of sinus node sensing in man.

Angina Pectoris↗

Electrophysiologic and electrocardiographic consequences of congestive heart failure.

In order to determine the effect of altered autonomic tone in patients with reduced left ventricular function and congestive failure on atrioventricular conduction, the refractory periods of the A-V conducting system were compared in forty-five patients with normal left ventricular function and fifteen patients with a left ventricular end-diastolic pressure greater than 12 mmHg and a left ventricular ejection fraction less than 50% with symptoms of congestive failure. All patients in the study had resting heart rates of 90 beats per minute or less. Patients with congestive failure were found to have a significant reduction in the functional refractory period of the A-V node (390 +/- 29 msec versus 430 +/- 38 msec; P less than 0.01) and the effective refractory period of the total A-V conducting system (275 +/- 34 msec versus 311 +/- 45 msec; P less than 0.01). In addition, patients with congestive failure had a higher incidence of aberrant conduction of premature atrial contractions (14 of 15 versus 22 of 45; P less than 0.01) and a significantly higher incidence of left bundle branch aberration (50% versus 20%; P less than 0.01). The results indicate significant facilitation of A-V nodal conduction in patients with congestive failure probably due to enhanced sympathetic activity and decreased parasympathetic inhibition. These findings may increase the ability of the clinician to understand electrophysiologic changes in congestive heart failure.

Atrioventricular Node↗

Mitochondrial function, oxygen extraction, epicardial S-T segment changes and tritiated digoxin distribution after reperfusion of ischemic myocardium.

This study examines the effect of 2 hours of reperfusion on transiently ischemic myocardium in pigs. Indexes of myocardial viability measured were mitochondrial function, oxygen extraction, epicardial S-T segment change and distribution of tritiated digoxin. Results were as follows: (1) Mitochondrial function was markedly impaired in the reperfused area after 60 minutes or more of coronary occlusion. The defect would seem to be a block in electron flow near site I, which can be partially bypassed with succinate. (2) An apparent inability of the reperfused myocardium to extract oxygen did not improve with 2 hours of reperfusion. (3) Epicardial S-T segment mapping suggested that necrosis occurred during reperfusion. (4) There was an altered distribution of tritiated digoxin in the reperfused area. The results show that reperfusion for 2 hours did not improve myocardial viability after 60 minutes or more of ischemia.

Adenosine Triphosphate↗

Altered refractory periods in patients with short P-R intervals and normal QRS complex.

To evaluate the refractory periods of the atrioventricular (A-V) conducting system in patients with a short P-R interval and normal QRS complex, 57 patients with a P-R interval of 110 to 280 msec were studied with His bundle recording and premature atrial stimulation at similar cycle lengths of 660 to 720 msec. In 13 patients with a short P-R interval (120 msec or less) the mean value for the functional refractory period of the A-V node was 368 plus or minus 36 msec (standard deviation), which was significantly lower (P smaller than 0.01) than the mean value of 415 plus or minus 50 msec in 36 patients with a normal P-R interval (between 120 and 200 msec) and the mean value of 492 plus or minus 57 msec in 8 patients with an increased P-R interval (200 msec or greater). Patients with a short P-R interval had a mean value for the effective refractory period of the A-V conducting system of 247 plus or minus 26 msec, which was significantly lower (P smaller than 0.01) than the mean values of 297 plus or minus 51 msec in patients with a normal P-R interval and 369 plus or minus 87 msec in patients with an increased P-R interval. The results identify a characteristic conduction abnormality that is compatible with a partial A-V nodal bypass or dual A-V nodal conduction pathways. The relation between the duration of the P-R interval and the regractory period may aid understanding of the clinical significance of the scalar electrocardiogram.

Adult↗