Comparative survival after permanent ventricular and dual chamber pacing for patients with chronic high degree atrioventricular block with and without preexistent congestive heart failure.

To determine whether survival after permanent ventricular demand (VVI) pacing differs from survival after permanent dual chamber (DVI or DDD) pacing in patients with chronic high degree atrioventricular (AV) block (Mobitz type II or trifascicular block), 132 patients who received a VVI pacemaker (Group 1) and 48 patients who received a DVI or DDD pacemaker (Group 2) were followed up for 1 to 5 years. There was no significant difference in sex distribution, mean age or incidence of coronary heart disease, hypertension, valvular heart disease, diabetes mellitus, stroke or renal failure between Groups 1 and 2. Overall, the predicted cumulative survival rate at 1, 3 and 5 years was 89, 76 and 73%, respectively, for Group 1 and 95, 82 and 70%, respectively, for Group 2. In patients with preexistent congestive heart failure, the predicted cumulative survival rate at 1, 3 and 5 years was 85, 66 and 47%, respectively, for Group 1 (n = 53) and 94, 81 and 69%, respectively, for Group 2 (n = 20). The 5 year predicted cumulative survival rate was significantly lower in Group 1 patients with preexistent congestive heart failure than in Group 2 patients with the same condition (p less than 0.02). There was no significant difference in 5 year cumulative survival rate between Groups 1 and 2 for patients without preexistent congestive heart failure. The results suggest that permanent dual chamber pacing enhances survival to a greater extent than does permanent ventricular demand pacing in patients with high degree AV block and preexistent congestive heart failure.

Atypical or nonanginal chest pain. Panic disorder or coronary artery disease?

Of 195 patients with atypical or nonanginal chest pain presenting in a cardiology clinic, 104 consented to be evaluated for anxiety disorders using a structured psychiatric interview. Thirty patients had histories of coronary artery disease (CAD). Fifty-nine patients in the sample (16 of those with CAD and 43 of those without CAD) fit diagnostic criteria for panic disorder (PD). Those without CAD and with PD were primarily women (mean age, 43 years) with predominantly nonanginal chest pain. Those patients with both CAD and PD were primarily men (mean age, 54 years) with predominantly atypical angina. Since PD has been shown to be readily responsive to pharmacologic intervention, this diagnosis should be considered in patients with atypical or nonanginal chest pain.

Effect of beta-blockade on right ventricular performance in patients with and without right ventricular dysfunction due to coronary artery disease.

To assess the effects of beta-blockade on right ventricular performance in patients with and without right ventricular dysfunction due to coronary artery disease, we performed radionuclide ventriculography on eight patients with normal right ventricular ejection fraction (RVEF greater than or equal to 35%) and 14 patients with mild to moderate right ventricular dysfunction (RVEF less than 35%) at rest. All patients had chronic stable angina pectoris, and nine patients had prior myocardial infarction. Radionuclide ventriculography was performed on placebo and during clinical beta-blockade (heart rate, 50 to 60 beats per minute and less than or equal to 20% increase in heart rate over baseline during stage I treadmill exercise, Bruce protocol) with the oral, cardioselective beta-blocking agent, betaxolol. The resting RVEF (mean +/- 1 SD) was 33% +/- 7% on placebo and 34% +/- 7% during clinical beta-blockade. Mean exercise RVEF was 40% +/- 8% on placebo and 39% +/- 8% during clinical beta-blockade. These differences were not statistically significant. Resting left ventricular ejection fraction ranged from 22% to 60% (mean, 42% +/- 8%). On placebo, one of eight patients with a resting RVEF greater than or equal to 35% had a normal exercise RVEF response (greater than or equal to 5% increment) whereas nine of 14 patients with resting RVEF less than 35% had normal exercise response. The discordant relationship between baseline RVEF and exercise response on placebo became less marked during clinical beta-blockade. We conclude that beta-blockade does not produce significant deterioration of right ventricular systolic function or right ventricular reserve either in patients with normal or in those with mild to moderately impaired resting right ventricular systolic function.

Effect of exercise on left ventricular systolic function and reserve in morbid obesity.

To assess the effect of exercise on left ventricular (LV) systolic function and reserve in morbid obesity, radionuclide left ventriculography was performed before and during supine, symptom-limited bicycle exercise in 23 patients whose body weight was greater than or equal to twice their ideal body weight. Echocardiography was performed before exercise. Resting LV ejection fraction was depressed in 13 patients and LV mass was increased in 10 patients. Exercise produced nonsignificant increases (of similar magnitude) in mean LV ejection fraction in the subgroups with normal and depressed resting LV ejection fraction. Exercise produced a significant increase in LV ejection fraction from 54 +/- 8 to 65 +/- 12% (p less than 0.005) in the subgroup with normal LV mass, but produced no significant change in LV ejection fraction in the subgroup with increased LV mass (53 +/- 10 at rest, 50 +/- 12% during exercise). Moreover, the LV exercise response (change in LV ejection fraction during exercise) in the subgroup with normal LV mass was significantly different from that in the subgroup with increased LV mass (p less than 0.005). There was a strong positive correlation between LV mass and the percent over ideal body weight (r = 0.912, p = 0.01) and a strong negative correlation between LV mass and LV exercise response (r = 0.829, p = 0.01). The results suggest that increased LV mass predisposes morbidly obese patients to impairment of LV systolic function during exercise.

Factors influencing left ventricular systolic function in nonhypertensive morbidly obese patients, and effect of weight loss induced by gastroplasty.

Heart rate and blood pressure were measured, and echocardiography was performed in 39 patients whose actual body weight was greater than twice their ideal body weight to identify factors influencing left ventricular (LV) systolic function in morbidly obese patients and assess the effect of weight loss on LV systolic function. Patients were studied before and after weight loss induced by gastroplasty. The study cohort was 133 +/- 8% overweight before weight loss and 39 +/- 7% overweight at the nadir of weight loss. Before weight loss, LV fractional shortening varied inversely with LV internal dimension in diastole (an indirect index of preload), LV end-systolic wall stress and systolic blood pressure (indexes of afterload). The weight loss-induced change in LV fractional shortening varied directly with the pre-weight loss LV internal dimension in diastole, LV end-systolic wall stress and systolic blood pressure, and inversely with the pre-weight loss LV fractional shortening. The weight loss-induced change in LV fractional shortening varied inversely with the weight loss-induced changes in LV end-systolic stress and systolic blood pressure. In patients with reduced LV fractional shortening (n = 14), weight loss produced a significant increase in LV fractional shortening that was accompanied by a significant decrease in LV internal dimension in diastole, LV end-systolic stress and systolic blood pressure. The results suggest that LV loading conditions have an important role in determining LV systolic function in morbidly obese patients. Improvement in LV systolic function in these patients is closely related to weight loss-induced alterations in LV loading conditions.

Acute and long-term effects of nifedipine on pulmonary and systemic hemodynamics in patients with pulmonary hypertension associated with diffuse systemic sclerosis, the CREST syndrome and mixed connective tissue disease.

Ten patients with pulmonary hypertension associated with diffuse systemic sclerosis (1 patient), the CREST syndrome (calcinosis cutis, Reynaud's phenomenon, esophageal dysmotility, sclerodactyl, telangiectasia) (6 patients) and mixed connective tissue disease (3 patients) were studied to assess the effect of oral nifedipine on pulmonary and systemic hemodynamics. Each patient underwent right-sided cardiac catheterization just before nifedipine administration. Thereafter, oral nifedipine was administered in 10 mg increments every 90 minutes until pulmonary vascular resistance normalized or a total dose of 30 mg was achieved. Hemodynamic measurements were obtained at 30-minute intervals for 3 hours, then hourly for 9 hours (acute study). Hemodynamic studies were repeated 3 to 6 months after the initial catheterization with the minimum dose of oral nifedipine (administered every 8 hours) required to achieve maximal reduction of pulmonary vascular resistance in the acute study (long-term study). In the acute study, oral nifedipine produced a significant decrease in mean pulmonary vascular resistance from 6.3 +/- 3.8 to 4.3 +/- 3.6 U (p less than 0.001). Similar changes in pulmonary vascular resistance were noted in the long-term study (n = 6). The results indicate that oral nifedipine is capable of producing an acute and sustained reduction in pulmonary vascular resistance in patients with pulmonary hypertension associated with diffuse systemic sclerosis, the CREST syndrome and mixed connective tissue disease.

Effect of beta blockade with betaxolol on left ventricular systolic function in chronic stable angina pectoris and left ventricular dysfunction.

To assess the effect of beta blockade on left ventricular (LV) performance in patients with LV dysfunction and stable angina pectoris, 18 subjects taking a placebo followed by incremental doses of the cardioselective beta-adrenergic blocking agent betaxolol (5, 10, 20, 40 and 80 mg/day) were studied. The study ended with the achievement of optimal clinical beta blockade (heart rate at rest 50 to 60 beats/min, a 20% or smaller increase in heart rate during stage 1 of symptom-limited treadmill exercise using the modified Bruce protocol). Optimal clinical beta blockade produced a decrease in mean frequency of angina, from 6.8 +/- 1.7 to 0.7 +/- 0.8 episodes per week (p less than 0.0005) and an increase in mean treadmill exercise capacity, from 3.1 +/- 1.7 to 7.7 +/- 2.8 minutes (p less than 0.0005). LV systolic function was assessed at rest and during symptom-limited exercise with radionuclide left ventriculography. Mean LV ejection fraction (EF) during therapy with placebo was 39 +/- 7% at rest and 40 +/- 8% at peak exercise. Mean LVEF during optimal clinical beta blockade was 43 +/- 11% at rest and 45 +/- 10% at peak exercise. Neither of these changes was statistically significant. No patient had clinical or radiographic signs of LV failure. The results suggest that optimal clinical beta blockade with betaxolol, in doses sufficient to significantly reduce the frequency of angina and improve exercise capacity in patients with stable angina pectoris and mild to moderate LV systolic dysfunction, does not cause significant deterioration of LV systolic function or produce LV failure.

Effect of exercise and cavity size on right ventricular function in morbid obesity.

To assess the effect of exercise and to determine the influence of the right ventricular (RV) internal dimension on RV systolic function in morbid obesity, M-mode and 2-dimensional echocardiography and radionuclide ventriculography were performed on 22 patients whose body weight was at least twice the ideal body weight and who had no clinical or laboratory evidence of underlying organic heart disease or pulmonary disease. RV ejection fraction was measured at rest and during peak supine bicycle exercise. RV exercise response was defined as the change in RV ejection fraction during peak exercise. There was a significant negative correlation between percent over ideal body weight and RV exercise response (r = 0.86, p less than 0.00005) and between RV internal dimension and RV exercise response (r = 0.60, p less than 0.005). There were significant positive correlations between resting RV and left ventricular (LV) ejection fraction (r = 0.56, p less than 0.01) and between RV and LV exercise response (r = 0.70, p less than 0.0005). The subgroup with a high-normal or enlarged RV internal dimension (greater than or equal to 2.0 cm, n = 10) experienced no significant change in RV ejection fraction with exercise, whereas the subgroup whose RV internal dimension was less than 2.0 (n = 12) experienced a significant increase in RV ejection fraction from 44 +/- 10% at rest to 58 +/- 11% at peak exercise (p less than 0.03). The results suggest that in morbidly obese individuals without underlying cardiopulmonary disease RV dilatation may predispose to RV systolic dysfunction and assessment of RV systolic function should optimally include evaluation of RV exercise response.

Cardiac morphology and left ventricular function in normotensive morbidly obese patients with and without congestive heart failure, and effect of weight loss.

To assess cardiac morphology and left ventricular (LV) function in normotensive morbidly obese patients with and without congestive heart failure (CHF) we performed a physical examination and obtained a transthoracic echocardiogram and cardiac Doppler studies before and after substantial weight loss in patients whose actual body weight was initially equal to or more than twice their ideal body weight and who were free from systemic hypertension and underlying organic heart disease. There were 24 patients with CHF, 14 of whom were studied after weight loss. There were 50 patients without CHF, 39 of whom were studied after weight loss. Compared to patients without CHF, those with CHF had significantly greater mean LV internal dimension in diastole, LV end-systolic wall stress, LV mass/height index values, left atrial dimension and right ventricular internal dimension values, significantly lower mean LV fractional shortening, and transmitral Doppler E/A ratio values, and significantly longer mean transmitral E-wave deceleration time and duration of morbid obesity than patients without CHF. Substantial weight loss in those with and without CHF produced comparable reductions in mean LV internal dimension in diastole, LV end-systolic wall stress, LV mass/height index, transmitral Doppler E-wave deceleration time, and left atrial dimension, and comparable increases in LV fractional shortening and transmitral Doppler E/A ratio. Linear regression analysis identified duration of morbid obesity as the strongest predictor of CHF (p <0.00000002). Thus, LV mass is greater and LV systolic function and diastolic filling are more impaired in normotensive morbidly obese subjects with CHF than in those without CHF. Duration of morbid obesity is the strongest predictor of CHF among the variables studied. Substantial weight loss produces comparable changes in cardiac morphology and function in those with and without CHF.

Panic disorder in patients with chest pain and angiographically normal coronary arteries.

Although patients with angiographically normal or near normal coronary arteries are at low risk for cardiac disease, several follow-up studies have shown that many continue to report recurrent chest pain associated with social and work dysfunction. Three diagnostic entities have been proposed to explain the morbidity of this group: microvascular angina, esophageal motility disorders and panic disorder. The purpose of this study was to test the hypothesis that panic disorder is found frequently in patients with chest pain who have normal epicardial vessels. Ninety-four subjects with angiographically normal coronary arteries were interviewed according to a structured psychiatric protocol within 24 hours of their catheterizations. Thirty-two (34%) fit Diagnostic and Statistical Manual of Mental Disorders (third edition, revised) criteria for current panic disorder. Because panic disorder can be effectively treated, physicians should consider this diagnosis in this group of patients. Current research findings suggest that panic disorder, microvascular angina and esophageal disorders may each form the basis for chest pain in approximately 25% of these patients. Miscellaneous problems account for the other 25%.

Relation of duration of morbid obesity to left ventricular mass, systolic function, and diastolic filling, and effect of weight loss.

Longer duration of morbid obesity is associated with higher LV mass, poorer LV systolic function, and greater impairment of LV diastolic filling. Weight loss-induced decreases in LV mass and improvements in LV systolic function and diastolic filling are due in part to favorable alterations in LV loading conditions.

Treatment of chronic symptomatic supraventricular bradyarrhythmias with transdermal scopolamine.

The management of symptomatic bradyarrhythmias can be challenging in patients in whom cardiac pacing is not indicated, such as in the terminally ill or severely demented. We applied a transdermal scopolamine patch on one such patient with resultant substantial improvement in his supraventricular bradyarrhythmia.

Short- and long-term hemodynamic effects of captopril in patients with pulmonary hypertension and selected connective tissue disease.

To assess the pulmonary and systemic hemodynamic effects of oral captopril in patients with connective tissue disease and pulmonary hypertension, we performed right heart catheterization in eight patients with diffuse systemic sclerosis, the CREST syndrome, or mixed connective tissue diseases prior to and immediately following administration of captopril (dose range 12.5 to 50.0 mg, short-term study). Four of these patients underwent repeat right heart catheterization after three to six months of oral captopril therapy (long-term study). In the short-term study, oral captopril produced a significant decrease in mean pulmonary vascular resistance from 6.2 +/- 3.6 to 4.6 +/- 3.8 units (p < 0.01). This was accompanied by a significant decrease in mean pulmonary artery pressure, mean blood pressure, mean systemic vascular resistance and a significant increase in cardiac output. Similar changes in pulmonary hemodynamics were noted in the long-term study. Thus, oral captopril is capable of producing an acute and sustained reduction in pulmonary vascular resistance in patients with pulmonary hypertension associated with the aforementioned connective tissue diseases.

Diminished short-term heart rate variability predicts inducible ventricular tachycardia.

PURPOSE: The purpose of this study is to determine whether short-term heart rate variability (HRV) can be used successfully to predict inducible ventricular tachycardia (VT). METHODS: A high-speed (300 mm/s) electrocardiographic recording was obtained in 32 patients in the supine position prior to programmed ventricular stimulation. Beat-to-beat RR intervals (in milliseconds) were derived from an 11-beat strip (10 RR intervals). Logistic regression was used to study the relationship between several variables and a dichotomous dependent variable (inducible, clinical, or electrocardiographic evidence of VT). RESULTS: Of 32 patients, 12 had inducible VT (inducible VT group) and 20 had no clinical or electrocardiographic evidence of VT (control group). Mean short-term HRV values were significantly lower in those with inducible VT than in the control group in all patients (25+/-15 ms, n=12 vs 67+/-22 ms, n=20; p<0.0001) and in patients with coronary artery disease or congestive heart failure or both (22+/-13 ms, n=11 vs 63+/-23 ms, n=11; p<0.0001). For the group as a whole, short-term HRV was < or =50 ms in 11 of 12 patients (92%) with inducible VT, but was < or =50 ms in only 3 of 20 control subjects (15%; p<0.001). As a result of a stepwise selection procedure conducted within the logistic regression, only the short-term HRV was found to be predictive of inducible VT (p<0.0001). CONCLUSION: Short-term HRV is significantly lower in subjects with inducible VT than in those without clinical or electrocardiographic evidence of VT. The probability of developing sudden death increases substantially when short-term HRV decreases below 50 ms.

Panic disorder in cardiology patients: a review of the Missouri Panic/Cardiology Project.

This paper reviews current evidence from several cardiology populations that suggests that panic disorder is prevalent and underdiagnosed. Cardiology patients with atypical angina, and no heart disease have a high likelihood of having panic disorder, as suggested by studies of two separate cardiology populations. That they resemble psychiatric populations with panic is suggested by their positive response to alprazolam. A panic disorder subtype, called non-fear panic disorder also appeared in about one-third of these cardiology panic patients. These patients have most of the panic symptoms but do not report fear during their episodes.

Mitral valve prolapse, panic disorder, and chest pain.

Mitral valve prolapse is a common cardiac disorder that can readily be diagnosed by characteristic auscultatory and echocardiographic criteria. Although many diseases have been associated with mitral valve prolapse, most affected individuals have the primary form of the disorder. Mitral valve prolapse is an inherited condition commonly associated with myxomatous degeneration of the mitral valve and its support structures. Complications of mitral valve prolapse, including cardiac arrhythmias, sudden death, infective endocarditis, severe mitral regurgitation (with or without chordae tendineae rupture), and cerebral ischemic events, occur infrequently considering the wide prevalence of the disorder. Panic disorder is a specific type of anxiety disorder characterized by at least three panic attacks within a 3-week period or one panic attack followed by fear of subsequent panic attacks for at least 1 month. It too is a common condition with a prevalence and age and gender distribution similar to that of mitral valve prolapse. Panic disorder and mitral valve prolapse share many nonspecific symptoms, including chest pain or discomfort, palpitations, dyspnea, effort intolerance, and pre-syncope. Chest pain is the symptom in both conditions that most commonly brings the patient to medical attention. The clinical description of chest pain in patients with mitral valve prolapse is highly variable, possibly reflecting multiple etiologies. Chest pain in panic disorder is usually characterized as atypical angina pectoris and as such bears resemblance to the chest pain commonly described by patients with mitral valve prolapse. Multiple investigative attempts to elucidate the mechanism of chest pain in both conditions have failed to identify a unifying cause. Review of the literature leaves little doubt that mitral valve prolapse and panic disorder frequently co-occur. Given the similarities in their symptomatology, a high rate of co-occurrence is, in fact, entirely predictable. There is, however, no convincing evidence of a cause-effect relationship between the two disorders, nor has a single pathophysiologic or biochemical mechanism been identified that unites these two common conditions. Until specific biologic markers for these disorders are identified, it may be impossible to do so. The lack of a proven cause-and-effect relationship between mitral valve prolapse and panic disorder and the absence of a unifying mechanism do not diminish the clinical significance of the high rate of co-occurrence between the two conditions. Primary care physicians and cardiologists frequently encounter patients with mitral valve prolapse and nonspecific symptoms with no discernible objective cause who fail to respond to beta-blockade. Panic disorder should be considered as a possible explanation for symptoms in such patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Validating studies for panic disorder in patients with angiographically normal coronary arteries.

This article describes validating studies for diagnosing panic disorder in some patients with angiographically normal coronary arteries (NCA) and chest pain. Psychiatric interviews of 94 such patients showed that 34% met the diagnostic criteria for panic disorder. Further studies showed that NCA patients with panic disorder were more disabled at 3.5-year follow-up, had more relatives with panic disorder, were more likely to suffer from major depression, and were more likely to respond to 35% CO2 challenge with panic symptoms. Because panic disorder is highly disabling but responds well to psychological and pharmacologic treatments, screening NCA patients in the cardiology population for this disorder is recommended.

Panic disorder, cardiology patients, and atypical chest pain.

Although patients with angiographically normal coronary arteries have low mortality, several studies have indicated that their social and work morbidity is high. Panic disorder appears to be a major contributor to the continuing chest pain in this population. There are also many chest pain patients appearing in cardiology clinics who also do not have heart disease but who are not given the opportunity to be evaluated for psychiatric disorders. Among those presenting with atypical or nonanginal chest pain, panic disorder represents a likely etiologic consideration. The fact that such patients do exist in cardiology populations is further substantiated by an open-label trial of alprazolam which demonstrated a positive effect in patients selected from those with atypical chest pain and no heart disease found to fit panic disorder criteria. These findings strongly support the increasing affiliation between cardiology and psychiatry and reinforce the belief that many problems of the heart may be problems of the mind/brain.

Cardiac conduction abnormalities and atrial arrhythmias associated with salicylate toxicity.

Cardiac side effects from aspirin are uncommon; however, severe acid-base imbalance, pulmonary edema, ventricular ectopic activity and cardiopulmonary arrest have been reported in patients with toxic serum salicylate concentrations. We saw a patient with salicylate toxicity who developed a variety of sinus and atrioventricular nodal conduction disturbances and atrial arrhythmias with a relatively low toxic serum salicylate concentration. The cardiac rhythm returned to normal as the serum salicylate concentration decreased, and results of subsequent electrophysiologic testing and Holter monitoring were normal. A low serum albumin level may have resulted in altered salicylate binding in this patient, thereby increasing the availability of unbound (active) drug for toxic effects.

Major depression in cardiology chest pain patients without coronary artery disease and with panic disorder.

104 patients in a cardiology clinic with atypical or non-anginal chest pain were studied through a structured clinical interview. 43 without coronary artery disease fit diagnostic criteria for panic disorder. 19 (44%) of this group reported a lifetime prevalence of major depression, nine (21%) current and ten (23%) past only. Nine reported that their major depressive episodes had preceded the onset of their panic disorder. On many self-report questionnaire scales the group with a lifetime history of major depression (n = 19) differed significantly from the group with no lifetime history of major depression (n = 24). These differences, however, could be attributed primarily to the group with current major depression. There appears to be a subgroup of panic disorder patients who have current major depression who are more symptomatic than those with panic disorder and past major depression and panic disorder alone. These findings also suggest that the association between panic disorder and depression may remain high outside of psychiatric settings.