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Biomedical subjects

V Mukerji

Publications and source records attributed to V Mukerji.

At least 37 records · Page 2Linked to original sources
PubMed1993

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.

Adult↗
PubMed1993

Substrate use by elderly men during walking and low-sit cycling.

To compare the cardiovascular and metabolic responses to different exercise modes, ten healthy, elderly men (aged 71.4 +/- 4.2 yr) walked and cycled in the low-sit position for 15 min each at 70% of peak heart rate. Fifteen minutes of recovery separated the exercise bouts. Analysis of expired air was used to calculate oxygen consumption (VO2), respiratory exchange ratio (RER), O2 pulse, total energy expenditure (TE) and fat oxidation (FO). Ratings of perceived exertion (RPE) were recorded for both legs and breathing. Each subject maintained similar heart rates on each of the exercise bouts (mean = 108 beats.min-1). No significant differences were found in VO2, O2 pulse and TE. RPE's were significantly lower during walking than cycling (P < 0.05). FO was 42% higher during walking than cycling (P < 0.05). These results suggest that although the cardiovascular response and TE use during these two modes are similar, elderly men burn more fat during walking than low-sit cycling.

Aged↗
PubMed1993

Chest pain and angiographically normal coronary arteries. Implications for treatment.

Approximately 20% to 30% of patients who undergo coronary arteriography for the evaluation of chest pain are found to have normal coronary arteries. These patients have a survival rate comparable to that of the normal population, yet they continue to complain of symptoms on extended follow-up, and about half of this group are disabled on account of chest pain. Once other clinically obvious disorders have been ruled out, common diagnostic considerations include microvascular angina, esophageal dysfunction, and perhaps fibromyalgia. Panic disorder, however, is the most common condition affecting these patients and can be diagnosed in at least one third of the group, with or without the presence of the other conditions mentioned. Appropriate diagnosis and treatment can reduce the psychosocial morbidity so frequently seen in these patients.

Chest Pain↗
PubMed1992

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.

Adult↗
PubMed1991

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.

Adult↗
PubMed1991

Follow-up status of patients with angiographically normal coronary arteries and panic disorder.

Cardiology patients with normal coronary angiography demonstrate continuing and substantial social, health, and work disability. We hypothesized that the diagnosis of panic disorder would mark those for whom continuing disability is most likely. We interviewed 72 such patients at the time of their normal angiogram, and then again an average of 38 months later. Those with panic disorder (n = 36) demonstrated significantly more disability at follow-up than did the other study patients. We conclude that those patients with normal angiograms who have panic disorder are more disabled than those who do not have panic disorder. Panic disorder in psychiatric samples has been shown to be highly treatable. Therefore, early identification and treatment of panic disorder in this group is likely to minimize the suffering associated with this condition.

Adult↗
PubMed1991

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)

Anxiety Disorders↗
PubMed1991

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.

Anxiety Disorders↗
PubMed1991

Signal-averaged electrocardiographic detection of terminal QRS deflection suggesting late potentials.

A terminal QRS deflection on a 12-lead electrocardiogram (previously described as peri-infarction block) most likely represents slowed conduction in a large area of myocardium near the infarct zone. We have described a patient with peri-infarction block, abnormal findings on signal-averaged electrocardiogram, and reentrant ventricular tachyarrhythmias. Our observation underscores the need to recognize the importance of terminal QRS deflections in the appropriate clinical situation.

Adult↗
PubMed1991

Effect of hemodialysis on left ventricular systolic function in the presence and absence of beta-blockade: influence of left ventricular mass.

To assess the effect of hemodialysis on the left ventricular (LV) systolic function in the presence and absence of beta blockade, we performed echocardiography just prior to and immediately after 4-hour maintenance hemodialysis in 38 patients with end-stage renal disease. The LV systolic function was assessed in subgroups with normal and increased LV mass in both the beta blockade group (n = 19) and the non-beta blockade group (n = 19). There was a significant negative correlation between LV mass and the dialysis-induced change in the mean velocity of LV circumferential fiber shortening (mean Vcf) in both the beta blockade group (r = -0.93; p less than 0.0005) and in the non-beta blockade group (r = -0.82; p less than 0.0005). The mean dialysis-induced change in mean Vcf in the subgroup with increased LV mass in the beta blockade group (-0.02 +/- 0.11 circumferences/s) was significantly lower than the mean dialysis-induced change in mean Vcf in the non-beta blockade group (+0.12 +/- 0.04 circumferences/s; p less than 0.0005). Thus, the coexistence of increased LV mass and beta blockade significantly impedes the expected improvement of LV systolic function associated with hemodialysis.

Adrenergic beta-Antagonists↗
PubMed1991

Coronary artery aneurysms--a case study and literature review.

Coronary artery aneurysms are detected with increasing frequency owing to the advent of coronary angiographies. Although most patients with coronary artery aneurysms are asymptomatic, manifestations of myocardial ischemia may occur. The case described herein serves as a basis for a discussion of the pathogenesis, clinical manifestations, detection, and treatment of coronary artery aneurysms.

Adult↗
PubMed1990

Panic disorder without fear in patients with angiographically normal coronary arteries.

By DSM-III-R criteria, patients may be diagnosed as having panic disorder without reporting the experience of intense fear. However, if such patients do not report subjective fear, they may be less likely to receive a panic diagnosis. The authors studied 32 subjects with angiographically normal coronary arteries who fit panic disorder criteria. A total of 13 (41%) reported no fear during their last major attack. These subjects were contrasted with those who did report fear. Few differences were found in group demographic data or responses to self-report questionnaires. We conclude that there appear to be few differences between the nonfear panic disorder subjects and those who do report fear. This conclusion awaits further support using challenge tests, medication trials, biological indices, alexithymia inventories, and family studies. The recognition of the existence of this subtype is likely to increase the number of patients receiving the panic disorder diagnosis in cardiology settings, in psychiatric settings, and in research projects using structured clinical interviews.

Adult↗
PubMed1990

Efficacy of betaxolol in the treatment of stable exertional angina pectoris: a dose-ranging study.

To assess the efficacy of oral betaxolol in the treatment of stable exertional angina pectoris and to determine the relationship between betaxolol doses/serum concentrations and clinical/hemodynamic responses the authors studied 24 patients prior to and following stepwise administration of 5, 10, 20, 40, and 80 mg doses. The major endpoint for the study was the achievement of clinical beta blockade (heart rate 50-60 beats/min and less than or equal to 20% rise in treadmill stage I heart rate). Betaxolol produced a decrease in mean angina pectoris frequency from 6.6 +/- 1.9 episodes/week with placebo to 0.2 +/- 0.5 episode/week during clinical beta blockade (p less than 0.00005). Mean treadmill exercise time increased from 3.1 +/- 1.7 min with placebo to 7.3 +/- 2.3 min with doses sufficient to reduce angina pectoris frequency greater than or equal to 75% (p less than 0.00005) and to 8.0 +/- 2.3 min during clinical beta blockade (p less than 0.00005). The mean doses of betaxolol required to produce a greater than or equal to 75% decrease in angina pectoris frequency and clinical beta blockade were 12 +/- 5 mg (range 5-40 mg) and 28 +/- 29 mg (range 5-80 mg) respectively. Mean serum concentrations associated with these clinical endpoints were 23.8 +/- 9.7 ng/mL and 59.7 +/- 54.0 ng/mL respectively. The results indicate that betaxolol, in widely ranging doses, is highly effective in reducing angina pectoris frequency and improving exercise capacity in patients with stable exertional angina pectoris.

Angina Pectoris↗
PubMed1990

Major depression and agoraphobia in patients with angiographically normal coronary arteries and panic disorder.

Patients with panic disorder and/or agoraphobia appearing in psychiatric settings report rates for lifetime major depression between 24% and 91%. Between 40% and 90% of patients with panic disorder in psychiatric populations report concomitant agoraphobia. A recent study of panic disorder subjects appearing in an outpatient cardiology clinic confirmed the strong link between panic and depression but found only a weak association between panic disorder and agoraphobia. In order to test the reliability of these outpatient cardiology findings, the authors studied major depression and agoraphobia in patients with angiographically normal coronary arteries and panic disorder. Twelve of the 32 (37.5%) panic disorder subjects reported a lifetime history of major depression (nine current, three past only). Only two of the 32 (six percent) reported any phobic avoidance. This study confirms the previous findings which suggest that major depression is common in cardiology populations with panic disorder and that phobic avoidance is uncommon in this group.

Adult↗
PubMed1990

Panic disorder in cardiology patients.

This paper reviews current evidence from several cardiology populations that suggests 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. Although evidence is less clear concerning the relationship between MVP and panic, it appears that patients referred to ECHO and found to have MVP are also likely to have panic. Three other populations deserving further study are patients with 1) pacemaker syndrome, 2) coronary artery disease with atypical angina and 3) certain arrhythmias.

Adult↗
PubMed1989

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.

Adult↗
PubMed1989

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.

Adult↗