Neil de Soyza

Reevaluation of electrocardiographic criteria for left, right and combined cardiac ventricular hypertrophy

Cardiac chamber weight was determined at necropsy in 323 men to develop correlative studies of electrocardiographic criteria for ventricular hypertrophy. Thirty recommended criteria for left ventricular (LV) hypertrophy, 10 for right ventricular (RV) hypertrophy, and combinations of both criteria for combined hypertrophy were evaluated. Four methods for electrocardiographic diagnosis of LV hypertrophy were derived: (1) a modification of the Romhilt-Estes point system; (2) the presence of any 1 of 3 criteria: (a) S V1 + R V5 or V6 greater than 35 mm, (b) left atrial abnormality, or (c) intrinsicoid deflection in lead V5 or V6 greater than or equal to 0.05 second; (3) a combination of any 2 criteria or of 1 criterion (above) plus at least 1 of the following 3 additional criteria: (a) left-axis deviation greater than -30 degrees, (b) QRS duration greater than 0.09 second, or (c) T-wave inversion in lead V6 of 1 mm or more; and (4) the use of a single criterion--left atrial abnormality. Sensitivity varied from 57 to 66% and specificity from 85 to 93% among these 4 methods. Myocardial infarction increased sensitivity of the foregoing methods, but the specificity was reduced. Method 2 is preferred for the electrocardiographic diagnosis of LV hypertrophy. Two methods were useful for right ventricular (RV) hypertrophy: (1) the use of any 1 of 4 criteria: (a) R/S ratio in lead V5 or V6 less than or equal to 1; (b) S V5 or V6 greater than or equal to 7 mm; (c) right-axis deviation of more than +90 degrees, or (d) P pulmonale; and (2) use of any 2 combinations of the foregoing criteria. Sensitivity ranged from 18 to 43% and specificity from 83 to 95%. Combined hypertrophy was best diagnosed using left atrial abnormality as the sole criteria of LV hypertrophy, plus any 1 of 3 criteria of RV hypertrophy: (a) R/S ratio in lead V5 or V6 less than or equal to 1, (b) S V5 or V6 greater than or equal to 7 mm, or (c) right axis deviation greater than +90 degrees.(ABSTRACT TRUNCATED AT 250 WORDS)

Ectopic Ventricular Prematurity and Its Relationship to Ventricular Tachycardia in Acute Myocardial Infarction in Man

In order to determine the role of the coupling interval of a premature ventricular contraction (PVC) in the development of paroxysmal ventricular tachycardia (PVT) during the early phase of acute myocardial infarction in man, 52 male patients with documented acute myocardial infarction had 24-hour Holter monitoring commenced within 24 hours of the onset of prolonged chest pain. Review of the tape recordings revealed that 27 patients had PVT documented, while 25 patients did not. Analysis of the data on the two groups showed that the frequency of PVCs, coupled PVCs, and accelerated idioventricular rhythm (AIVR) were found to be associated with a significantly increased incidence of ventricular tachycardia.The mean coupling interval of the PVCs initiating episodes of ventricular tachycardia was not significantly different from either the mean coupling interval of the isolated PVCs in the patients with PVT or the mean coupling interval of the PVCs in the patients without PVT. This suggests that the coupling interval of a ventricular ectopic is a poor predictor of ventricular tachycardia in the early phases of acute myocardial infarction.

Digoxin-quinidine interaction: Changes in canine tissue concentration from steady state with quinidine☆

Tissue concentrations of tritiated digoxin inthe dog are altered by simultaneous administration of quinidine. Serum levels rise as tissue concentration decreases significantly in all tissue except brain tissue, where an increase of 51 percent is noted over that of the control digitalized state. The digitalis toxicity associated with digoxin-quinidine interaction appears to be associated with rising brain levels of digoxin and falling levels in the myocardium. These findings suggest a neurally mediated form of toxicity with this interaction related to a change in the space of distribution. The question of possible loss of inotropic effect associated with diminished myocardial digoxin concentration requires further study.

Sensitivity of electrocardiographic criteria for left ventricular hypertrophy according to type of cardiac disease

The sensitivity of 30 electrocardiographic criteria for left ventricular (LV) hypertrophy, isolated or combined, was examined to determine the relation to the underlying disease. Patients with coronary artery disease (CAD), systemic hypertension, valvular heart disease and cardiomyopathy were evaluated. A cardiac partition technique was used to define ventricular hypertrophy. Single electrocardiographic criteria often showed high sensitivity for 1 disease state, but not for others. Precordial voltage criteria were most sensitive for those with hypertensive and valvular disease. A QRS axis of more than -30 degrees occurred most often in patients with CAD. Both left atrial abnormality and abnormal T-wave inversion of more than 1 mm in V6 occurred with a high sensitivity in general; however, T-wave inversion of more than 1 mm in V6 had a low sensitivity in cardiomyopathy. Methods using combinations of various electrocardiographic criteria improved sensitivity. Using these methods, sensitivity of the electrocardiogram for LV hypertrophy was excellent for patients with systemic hypertension and valvular heart disease and acceptable by usual standards for patients with CAD and cardiomyopathy. Because the use of a single criterion is often ineffective, methods using multiple electrocardiographic criteria to detect LV hypertrophy are recommended when the patients under study have diverse cardiac diseases.

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.

Ventricular Arrhythmia 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.

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.

Effect of propafenone on left ventricular ejection fraction

The effects of orally administered propafenone on ejection fraction (EF) determined by radionuclide angiography were studied in 2 groups of patients receiving different dosing regimens. Fourteen group A patients had no clinical evidence of left ventricular (LV) dysfunction and were not receiving digoxin therapy. In this group a mean daily dosage of 879 mg resulted in a decrease in resting LVEF from 52 +/- 9% to 48 +/- 11% (p less than 0.05). Eight group B patients had clinical radionuclide evidence of LV dysfunction and were receiving digoxin therapy. In this group, a daily dosage of propafenone of 600 mg/day resulted in no significant change in LVEF. No clinically significant effects on cardiac compensation were evident in either group. These data suggest a negative inotropic effect that is either related to propafenone dosage or at least partially attenuated by digoxin therapy. Further studies are necessary to define precisely the effects of propafenone on LV function.

Association of accelerated idioventricular rhythm and paroxysmal ventricular tachycardia in acute myocardial infarction

Although previous studies have suggested that accelerated idioventricular rhythm rarely coexists with paroxysmal ventricular tachycardia, this relation has not been systematically evaluated in acute myocardial infarction. To examine this relation, the frequency and characteristics of the two arrhythmias were analyzed by performing 24 hour Holter monitoring during the initial 24 hours of acute myocardial infarction in 52 successive patients. Twenty-four of these patients had documented accelerated idioventricular rhythm; 28 patients did not. Paroxysmal ventricular tachycardia occurred in 83 percent of patients with accelerated idioventricular rhythm but in only 18 percent of patients without this arrhythmia (P < 0.001). The results remained at the same level of significance whether paroxysmal ventricular tachycardia was defined by rates greater than 100, 120 or 140 beats/min. These findings suggest that accelerated idioventricular rhythm complicating acute myocardial infarction is not always benign and is frequently associated with more serious forms of ventricular arrhythmia.

The long-term suppression of ventricular arrhythmia by oral acebutolol in patients with coronary artery disease

The short-term efficacy of oral acebutolol was evaluated in 20 patients with coronary artery disease and frequent premature ventricular contractions (PVCs) by serial 24-hour Holter monitoring before and while the patients were receiving an average daily dose of 1,100 mg. of acebutolol for four weeks. Fifty-five percent of the 20 patients showed a greater than 70% PVC reduction from baseline values. The only serious side effect during short-term therapy was mild, reversible cardiac decompensation in one patient. The long-term safety and continued efficacy of acebutolol was then evaluated over the next 11 months in nine of the 11 patients showing greater than 70% PVC reduction at four weeks. Two-thirds of these nine patients continued to show greater than 80% PVC reduction from baseline values at 12 months. One patient developed alopecia during long-term therapy. The majority of patients not responding well to acebutolol at four weeks had an actual increase in PVCs on acebutolol therapy. We conclude that acebutolol produces long-term, effective reduction in PVCs without serious toxicity in the majority of patients with ventricular ectopy. However, this drug appears to either produce an excellent response or no response with regard to PVC control in most instances.