Influence of surgery on the natural history of rheumatic mitral and aortic valve disease

The rate of survival, the evolution of functional cardiac status and the incidence of major complications during a 5 year period were studied in 410 patients with rheumatic mitral or aortic valve disease, of whom 200 were treated medically and 210 by surgery. The 5 year survival rates in patients with various types of rheumatic mitral valve disease were similar (45 percent for those with mitral stenosis and 46 percent for those with mitral insufficiency or mixed mitral insufficiency and stenosis). The survival rate in patients with aortic valve disease was somewhat more favorable (64 percent).Mitral valvulotomy had the most positive influence on mortality. The 85 percent 5 year survival rate of patients who underwent this procedure was significantly higher than that of patients with medically treated mitral stenosis. In patients submitted to mitral and aortic valve replacement, the survival rate was also improved in comparison with data in the corresponding medically treated groups, but to a lesser degree (70 percent for aortic valve replacement and 60 percent for mitral valve replacement). In all surgically treated groups, initial operative mortality was the primary determinant of the rate of survival at the end of 5 years.Survivors of all surgical groups had appreciable improvement in cardiac functional classification and a remarkable reduction in the incidence of heart failure and atrial fibrillation. The incidence of infectious endocarditis was significantly reduced after mitral valvulotomy, as compared with the incidence in patients with medically treated mitral stenosis. Mitral and aortic valve replacement did not reduce the incidence of infectious endocarditis. The incidence of thromboembolic phenomena was favorably influenced by mitral valvulotomy and aortic valve replacement, but not by mitral valve replacement.     

Ventricular tachycardia: prediction of response to oral aprindine with intravenous aprindine

Aprindine was administered both intravenously and orally to 25 patients with ventricular tachycardia refractory to conventional antiarrhythmic agents to test the hypothesis that the response to intravenous aprindine predicts the response to oral aprindine. Ten patients had incessant ventricular tachycardia and 15 had paroxysmal sustained inducible ventricular tachycardia. Eleven patients (43 percent) had conversion to sinus rhythm with intravenous aprindine (nine with incessant and two with paroxysmal sustained ventricular tachycardia). Thirteen patients (all with paroxysmal sustained ventricular tachycardia) manifested slowing of the tachycardia without conversion, whereas in one patient with incessant ventricular tachycardia, the tachycardia became less frequent and nonsustained after intravenous aprindine. All 11 patients who had conversion to sinus rhythm with intravenous aprindine remained free of ventricular tachycardia during oral treatment with aprindine (at 2 weeks) and for a follow-up period of 2 to 38 months (mean 16 +/- 13). Of the 14 patients who did not have conversion to sinus rhythm with intravenous aprindine, 12 had spontaneous or inducible ventricular tachycardia, or both, at evaluation 1 to 2 weeks after initiation of oral aprindine. In conclusion, administration of intravenous aprindine to patients with ventricular tachycardia is helpful in predicting the subsequent response to oral aprindine. In addition, the pattern of ventricular tachycardia predicted the response to aprindine; patients with incessant ventricular tachycardia tended to respond, and those with paroxysmal sustained ventricular tachycardia tended not to respond.     

Dual atrioventricular nodal pathways: A benign finding in arrhythmia-free children with heart disease

The incidence and significance of dual atrioventricular (A-V) nodal pathways are described in 78 children with associated congenital or acquired heart disease. None of these patients had clinical or electrocardiographic evidence of arrhythmia. Dual A-V nodal pathways were observed in 35 percent of the preoperative group and in 33 percent of the postoperative group. Despite this substrate for A-V nodal reentry, supraventricular tachycardia was neither induced during electrophysiologic evaluation nor did it develop clinically over a follow-up period of 1 month to 15 years. It is concluded that dual A-V nodal pathways are common and may be a benign finding in arrhythmia-free children with heart disease.     

Contribution of the risk factor concept to patient care in coronary heart disease

This article deals with the question of whether or not the risk factor concept, a principal aspect of preventive cardiology, has contributed to patient care in coronary heart disease. The risk factors considered are plasma cholesterol, high blood pressure, smoking, diabetes and marked obesity. With the exception of plasma cholesterol and diabetes, all of these factors enhance myocardial oxygen consumption and thus, in the presence of coronary insufficiency, promote myocardial ischemia. Their modification is therefore good general medical practice, even if not related to coronary atherosclerosis. Diabetes needs adequate medical treatment in patients both with and without coronary atherosclerosis.Because of the occasional occurrence of spontaneous regression of coronary atherosclerosis and the morphologic and functional complexity of coronary artery pathology, it has never been and probably never will be demonstrated that lowering plasma cholesterol levels by diet or other means will cause regression of coronary atherosclerosis. It follows that modification or treatment of risk factors is implemented for good medical reasons but does not demonstrably or predictably affect coronary artery disease. It is concluded that the contribution of the risk factor concept to patient care in coronary heart disease has been, and still is, trivial.     

Long-term echocardiographic assessment of dilated cardiomyopathy in children

Left ventricular (LV) dimensions and function were assessed by echocardiography in 22 children with dilated cardiomyopathy. They had survived an initial episode of congestive heart failure in infancy for greater than or equal to 2 years. At the time of echocardiography, when they were 3 to 16 years old, 8 patients (Group 1) still had signs of dilated cardiomyopathy and 14 (Group 2) had lost all roentgenographic and electrocardiographic evidence of heart disease. All 8 patients in Group 1 (average follow-up 4.5 years) had significantly increased LV dimensions. The end-diastolic dimension averaged 144 +/- 18% of the normal value. Fractional LV shortening with systole was significantly reduced and averaged 23 +/- 3%. The E point-septal separation ranged from 7 to 17 mm (mean 12 +/- 4) and was far above the normal limit in all. Of the 14 patients in Group 2, seven (average follow-up 7 years) had normal ventricular dimensions and 7 (average follow-up 10 years) had LV dimensions larger than the upper range of the 95% prediction limit. In 6 of the latter patients the fractional LV shortening with systole was less than or equal to 31% and the E point-septal separation in excess of the upper limit of normal. These findings indicate that about half of the patients who had apparently recovered still had residual lesions as judged from the echocardiogram. In 6 patients in group 1, two-dimensional echo-cardiography allowed the visualization of a thickened endocardium. One of these 6 patients died. The echocardiographic image correlated well with the process of LV endocardial fibroelastosis found at necropsy.     

Restoration and maintenance of sinus rhythm after mitral valve surgery for mitral stenosis

The preoperative clinical, echocardiographic, hemodynamic and surgical data were studied from 40 consecutive patients with pure mitral stenosis and chronic atrial fibrillation who underwent surgical correction of mitral stenosis. After surgery, the patients had cardioversion of atrial fibrillation. The data of 24 patients who maintained sinus rhythm (SR) for more than 3 months (success group) were compared with the data of the 16 patients who failed to maintain SR for more than 3 months (failure group). The patients in the success group were younger (mean age 38 ± 12 vs 47 ± 13 years, p < 0.05), had symptoms for a shorter time (3.0 ± 4.3 vs 6.4 ± 5.0 years, p < 0.02) and had a smaller preoperative echocardiographic left atrial (LA) size (4.9 ± 0.9 vs 5.5 ± 1.0 cm, p < 0.03). The correlation between duration of SR after cardioversion (range 0 to 12 months) and the preoperative data were examined with the use of the “all-possible-subsets-regression” software. The best subset of predictors of successful cardioversion included echocardiographic LA size, functional capacity, duration of symptoms and echocardiographic left ventricular fractional shortening. Patients with symptoms for more than 3 years and echocardiographic LA size of more than 5.2 cm had low rate of successful cardioversion; in this subset of patients, postoperative cardioversion should be avoided.     

Hypertrophic cardiomyopathy after aortic valve replacement

The association of hypertrophic cardiomyopathy and aortic valve disease is well documented. However, the new development of the syndrome late after valve replacement has not previously been described. We present six cases, all occurring in women aged 50 to 71 years who had evidence of hypertrophic cardiomyopathy 3 to 5 years after successful valve replacement. The preoperative hemodynamic lesion was aortic stenosis in four and aortic regurgitation in two. Before operation no patient showed evidence of hypertrophic cardiomyopathy as judged by the absence of (1) asymmetric septal hypertrophy (the septal/posterior wall ratio was less than 1.4:1.0 in each case); (2) systolic anterior mitral valve motion; (3) obliteration of the left ventricular cavity on angiography; and (4) an intraventricular pressure gradient. After valve replacement no patient had significant aortic regurgitation or was hypertensive. Four patients subsequently had recurrence of symptoms including dyspnea in four, angina in three and syncope in two. The electrocardiogram revealed reappearance of left ventricular hypertrophy in four patients and left bundle branch block in one. The echocardiogram disclosed asymmetric septal hypertrophy in six (septal/posterior wall ratio greater than 1.8:1.0), systolic anterior motion in three and evidence of inflow obstruction in three. At cardiac catheterization an intraventricular gradient of 36 to 60 mm Hg was demonstrated at rest in three patients, on provocation in one patient; two patients showed no gradient. Angiograms showed obliteration of the left ventricular cavity in all six patients (ejection fraction 0.84 to 0.93). Two patients had coronary artery disease. No patient had an aortic transvalve gradient at rest or with exercise.     

Treadmill exercise testing in the Wolff-Parkinson-White syndrome

Graded treadmill exercise testing was performed in 54 patients with the Wolff-Parkinson-White syndrome and preexcitation (persistent in 36, intermittent in 9 and concealed in 9). Forty-eight patients had previous paroxysmal supraventricular arrhythmia (spontaneous or induced or both). At initiation of treadmill testing, the nine patients with intermittent and the nine with concealed preexcitation had normal conduction. None manifested preexcitation during exercise. Thirty-six patients had preexcitation at initiation of exercise; exercise produced no change in preexcitation in 2, partial normalization of the QRS complex in 16 (due to enhanced atrioventricular [A-V] nodal conduction), and total normalization of the QRS complex in 18 (due to enhanced A-V nodal conduction in 14 and to rate-dependent anomalous pathway block in 4). Exercise-provoked block of the anomalous pathway reflected prolonged anomalous pathway refractoriness, as measured with atrial stimulation. All 18 patients with either total or partial preexcitation at peak exercise manifested more than 1 mm flat or downsloping S-T segment depression. None had evidence of ischemic heart disease. None of the 54 patients manifested either paroxysmal supraventricular tachycardia or atrial fibrillation during or after treadmill exercise.Treadmill exercise testing in patients with preexcitation frequently produces partial or total normalization of the QRS complex due to enhanced A-V nodal conduction and, less commonly, total normalization due to rate-dependent block of the anomalous pathway. False positive S-T segment changes (suggesting ischemia) are always present in patients manifesting preexcitation during treadmill testing. Treadmill exercise testing in patients with preexcitation does not provoke paroxysmal supraventricular tachycardia or atrial fibrillation and is not useful as a provocative test for arrhythmia.     

Comparative actions of hydralazine, nifedipine and amrinone in primary pulmonary hypertension

The effects of 3 types of vasoactive agents, hydralazine, nifedipine and amrinone, were evaluated in 7 patients with primary pulmonary hypertension (PPH). Hemodynamic values were measured before and after drug administration in every patient. All drugs increased cardiac output and reduced both systemic and pulmonary resistance in the patients studied. Only nifedipine significantly reduced pulmonary artery (PA) pressure (6 +/- 5 mm Hg). In addition, it decreased pulmonary resistance to a greater degree than systemic resistance in 2 of the 7 patients, suggesting that nifedipine can cause selective pulmonary vasodilation in some patients. Hydralazine appeared to increase cardiac output and stroke volume by reducing systemic resistance. There was no evidence of direct pulmonary vasodilating effects; it decreased systemic resistance more than pulmonary resistance in every case. The increase in cardiac output from amrinone was secondary to a decrease in systemic arterial pressure with reflex tachycardia; stroke volume was unchanged. Amrinone had little pulmonary effect in all but 1 patient, in whom it substantially reduced PA pressure and pulmonary resistance. The mechanism of action of these 3 drugs in PPH differs. Nifedipine holds the most promise as an effective pulmonary vasodilator. A study of the effects of long-term administration of nifedipine in PPH is warranted.     

Effects of propranolol on anomalous pathway refractoriness and circus movement tachycardias in patients with preexcitation

Electrophysiologic effects of intravenous propranolol, 0.1 mg/kg, were evaluated in 18 patients with anomalous pathways utilizing intracardiac stimulation and recording. Fourteen patients had Wolff-Parkinson-White syndrome and four had concealed ventricular preexcitation. Anomalous pathway effective refractory period could be measured during the control period and after propranolol administration in nine patients and was 304 ± 7.5 (mean ± standard error of the mean) and 304 ± 8.3 msec, respectively (difference not significant). Ventricular paced 1:1 ventriculoatrial (V-A) conduction (reflecting retrograde anomalous pathway conduction) measured in 12 patients was intact during both the control period and after propranolol at rates of 170 to 200/min. Sustained paroxysmal supraventricular tachycardia was induced in 14 patients during the control period and in 10 after propranolol (in 4 of whom the tachycardia could not be sustained because of atrioventricular [A-V] nodal refractoriness). Mean cycle length of tachycardia in these 10 patients was 328 ± 18 (control) and 352 ± 19 msec (propranolol) (P < 0.01). The increase in tachycardia cycle length reflected an increase in A-V nodal conduction time (A-H interval).In conclusion: (1) Propranolol has an insignificant effect on both anterograde and retrograde anomalous pathway properties. (2) In most cases, propranolol does not interfere with induction of sustained circus movement tachycardia. However, it does produce a statistically significant but slight slowing of the rate of tachycardia. (3) In a minority of cases, propranolol inhibits induction of sustained paroxysmal supraventricular tachycardia by increasing A-V nodal refractoriness.     

Electrophysiologic demonstration of bilateral anomalous pathways in a patient with Wolff-Parkinson-White syndrome (type B preexcitation).

Pre- and postoperative electrophysiologic studies are described that were suggestive of two (right- and left-sided) anomalous atrioventricular (A-V) connections in a patient with type B Wolff-Parkinson-White syndrome and intractable arrhythmias, who underwent epicardial mapping and successful surgical ablation of the right-sided anomalous pathway. The presence of the right-sided anomalous pathway capable of both antegrade and retrograde conduction was suggested by the following observations: (1) Type B preexcitation on the surface electro-cardiogram; (2) maximal preexcitation and minimal stimulus-delta with low lateral right atrial pacing; (3) epicardial mapping of the atria and ventricles; and (4) disappearance of ventricular preexcitation after surgical ablation of the right-sided anomalous pathway. The presence of an additional left-sided anomalous pathway capable of only retrograde conduction (concealed on the surface electrocardiogram) was sugg-sted by the following observations: (1) Left to right retrograde atrial activation sequence during reentrant tachycardia and ventricular pacing at rapid rates and with coupled ventricular pacing postoperatively; (2) spontaneous conversion of wide ORS tachycardia utilizing the anomalous pathway for antegrade conduction to narrow QRS tachycardia with significant slowing in rate; and (3) smooth antegrade A-V nodal conduction curves with echo zone postoperatively. The demonstration of bilateral anomalous pathway in patients with preexcitation has important electrophysiologic and surgical implications.     

H-V interval in patients with bifascicular block (right bundle branch block and left anterior hemiblock). Clinical, electrocardiographic and electrophysiologic correlations.

Electrophysiologic studies were performed in 119 adults with chronic bifascicular block manifested by right bundle branch block and left anterior hemiblock. The H-V interval was normal in 86 patients and prolonged in 33. The following clinical variables were more frequent (P less than 0.05) in patients with a prolonged H-V interval: cardiac third sound, mitral systolic murmur, cardiomegaly on chest roentgenogram, congestive heart failure and cardiac functional class III or IV (New York Heart Association criteria). The following differences in the electrocardiographic and electrophysiologic findings were found: Patients with a prolonged H-V interaval had a longer mean P-R interval, QRS duration and A-H interval (P less 0.02). All patients were followed up prospectively in a cardiac conduction disease clinic after initial evaluation. The mean follow-up periods were (mean plus or minus standard error of the mean) 514 plus or minus 49 and 563 plus or minus 34 days for the patients with a prolonged and normal H-V interval, respectively. Progression of conduction disease occurred in three patients (4 percent) with a normal H-V interval and in four (12 percent) with a prolonged interval. The cumulative 3 year mortality rate for the entire group was 25 percent. The patients with a prolonged H-V interval had a higher cumulative 2 year mortality rate than those with a normal H-V interval but the difference was not statistically significant. In summary, a prolonged H-V interval was often associated with serious myocardial dysfunction and a high mortality rate. The risk of progression of conduction disease was slight with either a prolonged or a normal H-V interval during this relatively short follow-up period.     

Retrograde dual atrioventricular nodal pathways

Thirty-one (3.5 percent) of 887 studied patients had retrograde dual atrioventricular (A-V) nodal pathways, as manifested by discontinuous retrograde A-V nodal conduction curves (29 patients) or by two sets of ventriculoatrial (V-A) conduction intervals at the same paced cycle length (2 patients). All patients had A-V nodal reentrant ventricular echoes of the unusual variety induced with ventricular stimulation (25 patients had single, 2 patients had double and 4 patients had more than three ventricular echoes). The weak link of the reentrant circuit was always the retrograde slow pathway. Eleven of the 31 patients also had anterograde dual A-V nodal pathways (bidirectional dual pathways). Eight patients (26 percent) had spontaneous as well as inducible A-V nodal reentrant paroxysmal supraventricular tachycardia (of the unusual type in three and the usual type in five). In addition, three patients (10 percent) had only inducible supraventricular tachycardia (two of the unusual and one of the usual type).Retrograde dual A-V nodal pathways are uncommon. They are associated with the finding of at least single A-V nodal reentrant ventricular echoes (all patients), anterograde dual pathways (one third of patients) and A-V nodal reentrant paroxysmal supraventricular tachycardia of the usual or unusual variety (one third of patients).     

Radionuclide regurgitant index: Value and limitations

The radionuclide regurgitant index, defined as left ventricular/right ventricular stroke counts obtained from gated equilibrium studies, has been reported to predict the presence and severity of left-sided valve regurgitation. This study evaluated the radionuclide regurgitant index in 100 patients in whom left-sided valve regurgitation was angiographically graded (0 to 4+) with regard to most severe mitral or aortic regurgitation. Regurgitation was graded 0 in 44 of the 100 patients, 1+ in 22, 2+ in 8, 3+ in 6 and 4+ in 20.The radionuclide regurgitant index was 0.9 to 1.5 in 51 patients, 1.6 to 2.4 in 23 and 2.5 to 12.0 in 26. The mean radionuclide regurgitant index was 1.34 in the group with no regurgitation and 1.60 in those with 1+, 2.01 in those with 2+, 2.80 in those with 3+ and 3.85 in those with 4+ regurgitation. There was a significant difference (p <0.05) in the radionuclide regurgitant index between patients with no regurgitation and each group with regurgitation and between groups with regurgitation separated by two or more grades of angiographic regurgitation.Twelve patients had a discordant radionuclide regurgitant index; their index either predicted clinically significant or severe regurgitation when they had no or trivial regurgitation, or predicted no or trivial regurgitation when they had clinically significant regurgitation. Eight of 10 patients with a left ventricular ejection fraction of less than 0.30 had a discordant index (p < 0.0005). All three patients with mitral valve prolapse associated with frequent ventricular extrasystoles had a discordant index (p <0.0005).     

Value of lead V4R for recognition of the infarct coronary artery in acute inferior myocardial infarction

In 84 patients with an acute inferior wall myocardial infarction (MI) admitted within 10 hours after the onset of chest pain, a right precordial lead V4R electrocardiogram was recorded in addition to the standard 12-lead electrocardiogram. The presence or absence of ST-segment elevation in lead V4R was correlated with results of coronary angiography performed 2 to 26 weeks (mean 10) after MI. Patients were classified into 3 groups: (1) those with a critical stenosis or occlusion proximal to the first right ventricular (RV) branch (27 patients); (2) those with stenosis distal to the right ventricular branch of the right coronary artery (36 patients); and (3) those with stenosis in the left circumflex coronary artery (21 patients). The presence of ST-segment elevation greater than or equal to 1 mm in lead V4R has a sensitivity of 100% and a specificity of 87% for occlusion of the right coronary artery above the first RV branch; the predictive accuracy is 92%. Seven of 36 patients with a distal occlusion of the right coronary artery showed ST-segment elevation of 1 mm or more in lead V4R . The absence of ST-segment elevation greater than or equal to 1 mm in lead V4R excluded proximal occlusion of the right coronary artery. ST-segment elevation in lead V4R was not seen either in 29 of 36 patients with a distal occlusion of the right coronary artery or in all patients with an occlusion of the left circumflex artery. Recording of lead V4R within 10 hours after onset of acute inferior wall MI can give information rapidly about the vessel responsible for MI.(ABSTRACT TRUNCATED AT 250 WORDS)     

Procainamide-lnduced polymorphous ventricular tachycardia

Seven cases of procainamide-induced polymorphous ventricular tachycardia are presented. In four patients, polymorphous ventricular tachycardia appeared after intravenous administration of 200 to 400 mg of procainamide for the treatment of sustained ventricular tachycardia. In the remaining three patients, procainamide was administered orally for treatment of chronic premature ventricular contractions or atrial flutter. These patients had Q-T prolongation and recurrent syncope due to polymorphous ventricular tachycardia. In four patients, the arrhythmia was rapidly diagnosed and treated with disappearance of further episodes of the arrhythmia. In two patients, the arrhythmia degenerated into irreversible ventricular fibrillation and both patients died. In the seventh patient, a permanent ventricular pacemaker was inserted and, despite continuation of procainamide therapy, polymorphous ventricular tachycardia did not reoccur. These seven cases demonstrate that procainamide can produce an acquired prolonged Q-T syndrome with polymorphous ventricular tachycardia.     

Aprindine-induced polymorphous ventricular tachycardia

Five cases of aprindine-induced polymorphous ventricular tachycardia (torsade de pointes) are presented. In four cases, polymorphous ventricular tachycardia appeared after the oral administration of 400 mg of aprindine. One patient had mild hypokalemia at the time of polymorphous ventricular tachycardia so that a direct cause and effect relation between the drug and the tachycardia cannot be established. All five patients manifested Q-T prolongation and recurrent syncope due to polymorphous ventricular tachycardia. In all five, polymorphous ventricular tachycardia subsided once administration of aprindine was discontinued.     

Paroxysmal atrial fibrillation in the wolff-parkinson-white syndrome

Eighty-eight patients with preexcitation were studied to determine how 30 patients with documented spontaneous paroxysmal atrial fibrillation differed from 58 patients without this arrhythmia. Inducible reentrant tachycardia was present in 23 (77 percent) of the 30 patients with, versus 28 (48 percent) of the 58 patients without, atrial fibrillation (p < 0.025). Heart disease was present in 13 (43 percent) of the 30 patients with, versus 15 (26 percent) of the 58 patients without, atrial fibrillation (not significant). Inducible reentrant tachycardia or heart disease, or both, were present in 29 (97 percent) of the 30 patients with, versus 34 (59 percent) of the 58 patients without, atrial fibrillation (p < 0.0005).Of 51 patients with inducible reentrant tachycardia, 23 patients with atrial fibrillation did not differ from 28 patients without this arrhythmia with respect to clinical features and atrial, sinus nodal, or anomalous pathway properties, or cycle length of induced reentrant tachycardia. Spontaneous degeneration of induced reentrant tachycardia to atrial fibrillation was observed in 6 (26 percent) of 23 patients with, versus none of 28 patients without, atrial fibrillation (p < 0.025).In summary, patients with preexcitation and documented spontaneous paroxysmal atrial fibrillation almost always have inducible reentrant tachycardia or heart disease, or both. It is likely that in many patients with inducible reentrant tachycardia, spontaneously occurring reentrant tachycardia relates to induction of atrial fibrillation. However, it is unclear why some patients with inducible reentrant tachycardia have atrial fibrillation and others do not. In many patients with organic heart disease, atrial fibrillation could relate to hemodynamic changes.