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Biomedical subjects

K D Chadda

Publications and source records attributed to K D Chadda.

At least 37 records · Page 2Linked to original sources
PubMed1977

Significance and treatment of nocturnal angina preceding myocardial infarction.

The presence of nocturnal angina and congestive heart failure within the month prior to admission was evaluated in the 174 patients with acute myocardial infarction. Heart size was evaluated radiographically at the time of admission. Twenty-three patients (13 per cent) experienced nocturnal angina. The incidence of nocturnal angina was significantly higher in those with anterior myocardial infarction (p less than 0.005) and subendocardial infarction (p less than 0.02) when compared with patients with inferior MI. Congestive heart failure was more common prior to admission in those with nocturnal angina (9/23) as opposed to those without (3/141) (p less than 0.001). Cardiomegaly was seen in 9/23 patients with nocturnal angina and 22/141 without (p less than 0.02). We conclude that the presence of nocturnal angina in those who develop MI increases the likelihood that the infarction will be either anterior or subendocardial rather than inferior. The association of nocturnal angina and congestive heart failure to anterior myocardial infarction is probably due to more severe and probably significant left coronary artery disease.

Acute Disease↗
PubMed1977

Follow-up studies in patients with right bundle branch block and left anterior hemiblock: significance of H-V interval.

Thirty-eight patients with right bundle branch block and left anterior hemiblock who had undergone His bundle recordings were prospectively followed for development of heart block. Twenty-five were male and thirteen female. Their ages ranged from 35 to 92 with an average age of 74 years. The mean follow-up period was 28.5 months (range 2-52 months). The H-V interval was 55 msec or less in 17 patients (Group A), between 56 and 75 msec in 13 (Group B), and more than 75 msec in eight (Group C). Ten patients (26%) died during the follow-up period. Of these, three were in Group A (mortality rate 8% per year), three in Group B 10% per year), and four in Group C (21% per year). None of the deaths in Groups A and B were sudden, while one possible sudden death occurred in Group C. Mode of death in one patient each from Groups B and C remained unknown. Heart block was not seen in any patient from Group A and B, while two patients from Group C progressed to complete heart block during the follow-up period. It is concluded that patients with right bundle branch block and left anterior hemiblock with prolonged H-V intervals tend to show a higher mortality when compared to those with normal H-V intervals. A definite risk of heart block exists in patients with H-V intervals of more than 75 msec.

Adult↗
PubMed1976

Chronic His bundle block. Clinical, electrocardiographic, electrophysiological, and follow-up studies on 16 patients.

This report describes 16 patients with block within the His bundle seen over a period of 55 months. Ten were women and 6 men, with an average age of 76 years, range, 42 to 98 years. All patients had His bundle recordings showing split His bundle potentials (H and H) (13 patients) or narrow QRS with block distal to the His bundle potential (3 patients). Of the 16 patients, 10 had complete heart block, 4 second degree AV block (2 patients with Mobitz type II, and 2 with 2:1), and 2 first degree AV block. Ten patients had a narrow QRS in the conducted beats or escape rhythms. Intravenous atropine (1 to 2 mg) had a variable effect on AV conduction and the rate of the escape rhythm. Twelve patients have had a permanent pacemaker implanted. During the follow-up period, 10 patients died 1 to 31 months from the time of initial examination. The remaining 6 patients (5 with pacemaker) are alive 3 to 58 months later.

Adult↗
PubMed1976

Incidence and significance of left anterior hemiblock complicating acute inferior wall myocardial infarction.

The hospital course and serial vectorcardiograms of 56 consecutive patients with acute inferior wall myocardial infarction were reviewed. Left anterior hemiblock (LAH) complicating inferior wall myocardial infarction was diagnosed by vectorcardiographic criteria. Seven patients (12.5%) developed LAH between the first and third hospital day, while 49 patients did not. There was no significant difference between these two groups when compared for age, sex, incidence of congestive heart failure, atrial and ventricular arrhythmias, atrioventricular (A-V) block, hospital mortality, and previous hypertension, diabetes mellitus, and myocardial infarction. We conclude that LAH is a relatively common complication of acute inferior wall myocardial infarction, with no apparent effect on the clinical course.

Acute Disease↗
PubMed1976

The natural history of trifascicular disease following permanent pacemaker implantation. Significance of continuing changes in atrioventricular conduction.

Seventy-two patients with trifasicular disease were followed for an average of 40 months following permanent pacemaker insertion. The indications for pacemaker insertion were either electrocardiographic evidence of complete heart block with a wide QRS escape complex or a pattern of bifasicular block with either periods of Mobitz type II atrioventricular (A-V) block or a documented history of syncope. The patients were then divided into three groups depending on subsequent change in A-V conduction. There were 31 (43%) patients with no change in A-V conduction, 17 (24%) with increasing A-V block, and 24 (33%) with decreasing A-V block. The characteristics of these three groups, including age and sex distribution, were compared and found to be similar. The incidence of previous transmural myocardial infarction as determined by electrocardiographic criteria was higher in the group with decreasing block. Survival curves showed a significantly decreased probablity of surviving for those with decreasing block compared to both those with increasing block and those with no charge in conduction (P less than 0.03). We conclude that the probability of long-term survival was less in the group with decreasing block. This finding may be related to the greater prevalence of coronary heart disease in the patients.

Aged↗
PubMed1976

Sick sinus syndrome requiring permanent pacemaker implantation in a patient with mirror-image dextrocardia.

A patient with the sick sinus syndrome accompanying mirror-image dextrocardia which was associated with double superior venae cavae and an absent inferior vena cava is presented. A permanent transvenous demand pacemaker was inserted because of repeated episodes of dizziness and a documented 31/2-second period of asystole. Precise knowledge of the venous system and the location of the apex of the right ventricle was necessary prior to permanent pacemaker implantation.

Arrhythmia, Sinus↗
PubMed1976

Heart block complicating acute inferior wall myocardial infarction.

Heart block was noted in 60 (35 complete and 25 second-degree) of 410 patients with acute inferior wall myocardial infarction. This group with heart block was compared to a control group of 30 patients with acute inferior wall infarction without heart block. The incidences of prior myocardial infarction and hypertension, in addition to the highest level of serum creatine phosphokinase and a maximum degree of ST-segment elevation in the inferior leads, were all greater in patients with heart block, as compared to the controls. The incidences of various complications, including dizziness and syncope, transient hypotension, cardiogenic shock, and congestive heart failure, were also higher in the group with heart block, while sinus nodal distrubances and atrial arrhythmias occurred with equal frequency. The mortality in those with heart block was 28 percent compared to 13 percent for the control. It is concluded that patients with heart block complicating acute inferior myocardial infarction have a greater amount of myocardial necrosis, a higher incidence of complications, and a higher mortality. Insertion of a temporary pacemaker should be considered when specific indications are present and not routinely.

Acute Disease↗
PubMed1975

Transient atrioventricular standstill. Etiology and management.

Four patients with different clinical conditions had transient cardiac standstill for periods of up to 22.5 seconds. All patients showed signs of cerebral ischemia and required cardiac resuscitation. In one patient, the standstill was thought to be the result of a transient increase in the vagal tone, and no long-term therapy was required. In the second patient, cardiac standstill occurred during hospitalization for impending myocardial infarction. Coronary arteriography followed by coronary artery surgery was performed, and there was no further episodes of standstill. In the third patient, standstill was probably related to long-term ingestion of propranolol hydrochloride, and was not observed after this medication was discontinued. In the fourth patient, standstill was the result of the sick sinus syndrome, and a permanent pacemaker was inserted. Standstill of both atria and ventricles may occur under different clinical settings, and management of arrhythmia should be guided by thf etiology of the arrhythmia.

Adult↗
PubMed1975

Digitalis in experimental acute myocardial infarction. Differential effects on contractile performance of ischemic, border and nonischemic ventricular zones in the dog.

The effects of digoxin priming dose of 0.04 mg/kg body weight followed by infusion of 0.02 mg/kg per min) on local tension and length characteristics of the nonischemic, border and ischemic left ventricular zones were studied in 30 dogs using Walton-Brodie strain gauge arches and mercury-in-Silastic segment length gauges. Total tension in the nonischemic zone increased to 130.9 plus or minus 5.3 percent (P smaller than 0.001) of the control level in association with parallel changes in preejection and ejection tension and rate of rise of tension when infusion of digoxin was instituted 15 to 30 minutes after ligation. Consistent increases in tension variables were noticed when infusion of digitalis was initiated 45 to 60 minutes or 2 to 3 hours after ligation. Segment length remained unchanged. In the border zone, total tension decreased to 68.9 plus or minus 5.9 percent (P smaller than 0.01) after infusion of digitalis. When infusion of digitalis was instituted 45 to 60 minutes or 2 to 3 hours after occlusion, similar increases in total tension and other tension variables were seen. Segment length again showed no significant changes. There was an increase in total tension in 5 of the 12 ischemic zones studied when digitalis was infused 15 to 30 minutes after coronary arterial ligation, whereas a consistent (3 to 5 percent) decrease in tension was observed when infusion of digitalis was instituted 45 to 60 minutes and 2 to 3 hours after coronary occlusion. There was no increase in segment length. In summary, digitalis uniformly increased contraction of the nonischemic and border zones after coronary arterial ligation, but the effects on contraction and aneurysmal bulging in the ischemic zone were minimal.

Animals↗
PubMed1975

Refractory reentrant atrial tachycardia. Successful treatment with a permanent radio frequency triggered atrial pacemaker.

This 68 year old man had recurrent episodes of paroxysmal atrial tachycardia, probably due to chronic pericarditis, persisting over a 7 year period. These episodes were resistant to all conventional medical therapy and at times produced ischemic chest pain. There was no evidence of Wolff-Parkinson-White syndrome either on the standard electrocardiogram or on the His bundle electrogram performed with atrial pacing. Rapid atrial pacing at a rate of 200/min was found to promptly terminate the tachycardia and restore normal sinus rhythm. Because of the refractoriness of the patient's tachycardia, in addition to the presence of ischemic chest pain during these episodes, a permanent radio frequency triggered atrial pacemaker was inserted which enables him to initiate rapid atrial pacing by pressing an external control. The patient has been maintained on antiarrhythmic medications in an attempt to decrease the frequency of these episodes; during an 8 month follow-up period, he has done well with approximately one episode of tachycardia each month requiring radio frequency atrial pacing for termination.

Aged↗
PubMed1975

Bradycardia-hypotension syndrome in acute myocardial infarction. Reappraisal of the overdrive effects of atropine.

Sixty-eight (17 per cent) of 380 patients with acute myocardial infarction had the bradycardia-hypotension syndrome (ventricular rate below 60/min and systolic blood pressure less than 100 mm Hg) during the first 24 hours of admission to a large general hospital. In 61 of the 68 patients, the administration of atropine significantly increased the heart rate (from 46 plus or minus 14 to 79 plus or minus 12/min) (p less than 0.01) and systolic blood pressure (from 70 plus or minus 15 to 105 plus or minus 13 mm Hg) (p less than 0.001). In 26 of the 68 patients, ventricular premature complexes decreased from 9.4 plus or minus 3/min to 2.4 plus or minus 0.7/min (p less than 0.001) after the administration of atropine. It is concluded that the bradycardia-hypotension syndrome is not an uncommon complication following acute myocardial infarction and that selected doses of atropine may have a beneficial effect without significant complications.

Acute Disease↗
PubMed1975

Incidence and description of accelerated ventricular rhythm complicating acute myocardial infarction.

One hundred and nineteen episodes of accelerated ventricular rhythm (less than 125/min) were noted in 37 patinets with acute myocardial infarction during a 1 year period. The incidence was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia (less than 125/min) were noted in 16 of these patients. Eighteen patients had anterior myocardial infarction and 19 inferior myocardial infarction. The mechanism of onset of accelerated ventricular rhythm was classified as escape in 65 episodes. Ventricular premature beats were noted close to episodes of accelerated ventricular rhythm in 31 patients and fast ventricular tachycardia in 14 patients. The morphology of accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients and similar to the fast ventricular tachycardia in 12. In 11 patinets the morphology of ventricular premature beats, accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm is a relatively common complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time, and the instances of two arrhythmias having common rate multiples, suggest that at least in some instances accelerated ventricular rhythm may represent an ectopic focus with exit block.

Adult↗
PubMed1975

Long-term survival of patients with incomplete bundle-branch block complicating acute myocardial infarction.

Electrocardiograms and His bundle electrograms were reviewed in 28 patients with incomplete bilateral bundle-branch block complicating acute myocardial infarction. All had a His bundle electrogram at the time of pacemaker insertion; 10 had a second one. Of 23 patients with an initially abnormal HV interval (55 ms or greater), 15 died (65%), while only one died (20%) in the group of 5 with a normal HV interval. This difference is not statistically significant. Sequential His bundle electrograms were done in 6 of the 8 survivors with an initially abnormal HV interval, and 4 showed 10 to 15 ms decrease in HV interval. The disappearance of incomplete bilateral bundle-branch block occurred significantly more often in patients who survived (7 of 12) when compared with those who did not survive (2 of 16) (P less than 0.05). It is concluded that long-term survival is po-sible after incomplete bilateral bundle-branch block complicating acute myocardial infarction. The characteristics of the survivors include an initially normal HV interval, transient incomplete belateral bundle-branch block and a decreasing HV interval if it were initially abnormal.

Acute Disease↗
PubMed1975

Corrected sinus node recovery time. Experimental physiologic and pathologic determinants.

To determine the factors affecting reproducibility of sinus node recovery time, the effects of basic pacing rate, pacing duration, milliamperage, vagal and beta-adrenergic stimulation, and sinud node injury, as well as its instantaneous and daily reproducibility, were studied in 36 anesthetized dogs. Corrected sinus node recovery time (CSNRT) showed a mean variation of 9.8 plus or minus 0.4 msec at an atrial pacing rate of 200 beats/min and 29.8 plus or minus 8 msec at an atrial pacing rate of 140 beats/min (P smaller than 0.05). CSNRT increased progressively from 55.4 plus or minus 10 msec to 103.7 plus or minus 13 msec with increase in pacing rate from 140 beats/min to 200 beats/min. It was reproducible when atrial pacing was carried out for 1-5 min, although a wide variation (10-30 msec) was seen from 7-60 minutes (P smaller than 0.05). This measurement was reproducible on two consecutive days and was unaffected by changes in milliamperage. Vagal stimulation consistently prolonged the CSNRT while beta-adrenergic stimulation decreased it from 132.9 plus or minus 34.5 msec to 50.0 plus or minus 6.5 msec. Sinus node injury consistently prolonged CSNRT at all paced rates. In summary, CSNRT is reproducible only if the same pacing rate and duration are utilized. Since vagal stimulation and sinus node injury prolong this measurement while beta-adrenergic stimulation shortens it, an "abnormal" CSNRT should be assessed in terms of the possible influence of the autonomic nervous system as well as sinus node dysfunction per se.

Animals↗