Left ventricular mass and systolic function in human immunodeficiency virus-infected patients after weight loss.

Transthoracic echocardiography was performed on 27 patients with human immunodificiency virus after weight loss and in 20 lean controls. Left ventricular mass index was significantly higher and left ventricular fractional shortening was significantly lower in patients with human immunodificiency virus after weight loss than in lean, normal controls.

Factors predicting coronary artery disease in patients with giant negative T waves.

Seventy-four patients with giant negative T waves were studied to determine which electrocardiographic variables predicted the presence of coronary artery disease. The absence of left ventricular hypertrophy and the presence of symmetric T-wave inversion predicted coronary artery disease.

Fourier transform infrared spectrometry: a versatile technique for real world samples.

The versatility of FTIR spectrometry was explored by considering a variety of samples drawn from industrial applications, materials science and biomedical research. These samples included polymeric insulators, bauxite ore, clay, human hair and human skin. A range of sampling techniques suitable for these samples is discussed, in particular FTIR microscopy, FTIR emission spectroscopy, attenuated total reflectance and photoacoustic FTIR spectrometry. The power of modern data processing techniques, particularly multivariate analysis, to extract useful information from spectral data is also illustrated.

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.

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.

Influence of left ventricular mass on left ventricular diastolic filling in normotensive morbid obesity.

To identify factors influencing left ventricular (LV) diastolic filling in patients with morbid obesity, we performed transthoracic and Doppler echocardiography on 50 subjects whose actual body weight was > or = twice their ideal body weight and on 50 normal lean control subjects. The transmitral Doppler E/A ratio and E wave deceleration half-time were used to assess LV diastolic filling. Significant negative correlations were seen between the E/A ratio and the LV internal dimension in diastole (r = 0.819, p = 0.0001), systolic blood pressure (r = 0.751, p = 0.0001), LV end-systolic wall stress (r = 0.782, p = 0.0001), and LV mass/height index (r = 0.901, p = 0.0001). Significant positive correlations were seen between the E wave deceleration half-time and the LV internal dimension in diastole (r = 0.743, p = 0.0001), systolic blood pressure (r = 0.789, p = 0.0001), LV end-systolic wall stress (r = 0.828, p = 0.0001), and LV mass/height index (r = 0.831, p = 0.0001). No correlation was seen between diastolic blood pressure and either index of LV diastolic filling. Thus increasing LV mass is associated with progressive impairment of LV diastolic filling in morbidly obese individuals. The aforementioned alterations in LV loading conditions may contribute to impairment of LV diastolic filling directly or by increasing LV mass.

Interrelationship of left ventricular mass, systolic function and diastolic filling in normotensive morbidly obese patients.

OBJECTIVE: To determine the interrelationship of left ventricular (LV) mass, systolic function and diastolic relaxation in morbidly obese subjects. METHOD: We obtained echocardiograms (M-mode, two dimension) and cardiac Doppler studies (pulse wave, continuous wave colour flow) on 50 subjects whose actual body weight was > or = twice ideal body weight. LV mass/height index was calculated from echocardiographic data (Penn Convention). LV systolic function was assessed by calculating LV fractional shortening. LV diastolic filling was assessed by measuring the transmitral Doppler E/A ratio and the transmitral E wave deceleration time. RESULTS: There were significant positive correlations between LV mass/height index and the LV internal dimensions in diastole, systolic blood pressure, LV end-systolic wall wall stress and the transmitral E wave deceleration time. There were significant negative correlations between LV mass/height index and both LV fractional shortening and the transmitral Doppler E/A ratio. There were significant negative correlations between LV fractional shortening and the LV internal dimension in diastole, systolic blood pressure LV end-systolic wall stress and the transmitral E wave deceleration time. There was a significant positive correlation between LV fractional shortening and the transmitral Doppler E/A ratio. There were significant positive correlations between the transmitral E wave deceleration time and LV internal dimension in diastole, systolic blood pressure and LV end-systolic wall stress. There were significant negative correlations between the transmitral Doppler E/A ratio and the aforementioned variables. CONCLUSIONS: Unfavourable alterations in LV loading conditions contribute to the development of LV hypertrophy and impairment systolic dysfunction in morbidly obese subjects. Increasing LV mass and altered loading conditions may synergistically contribute to impairment of LV diastolic filling in such individuals.

Sweet taste (dysgeusia). The first symptom of hyponatremia in small cell carcinoma of the lung.

Three patients with small cell carcinoma of the lung presented with a persistent unpleasant sweet taste as their initial and only symptom. On further evaluation, they were found to have hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone. In each case, resolution of the sweet taste paralleled an increase in serum sodium concentration after water restriction alone. Linkage of the sweet taste with a low serum sodium concentration strongly implicates hyponatremia--rather than tumor, antidiuretic factor, medications, or chemotherapy--as the central mechanism responsible for this previously unreported (to our knowledge) sentinel symptom of small cell carcinoma of the lung.

Atrial wall tension changes and the release of atrial natriuretic factor on relief of cardiac tamponade.

Cardiac tamponade causes elevation and equalization of cardiac filling pressures, sodium and water retention, and a paradoxically low plasma atrial natriuretic factor (ANF) concentration despite increased intraatrial pressures. Recent reports suggested that plasma ANF concentrations rise after relief of tamponade. The purposes of the present study were (1) to determine the time course and extent of ANF release on relief of cardiac tamponade; (2) to measure the atrial transmural wall pressures, atrial sizes, and atrial wall tension changes associated with relief of tamponade; and (3) to determine the biologic activity of elevated plasma ANF during and after relief of tamponade. We sampled blood for ANF and cyclic guanosine monophosphate (cGMP) immediately before and up to 24 hours after relief of cardiac tamponade in 10 patients. Atrial and pericardial pressures were measured immediately before and shortly after pericardiocentesis, and atrial dimensions were determined by two-dimensional echocardiography before and within 1 hour after the tap. Urine volumes were measured in 8-hour increments before and after the procedure. Relief of cardiac tamponade was associated with a prompt and massive increase in plasma ANF concentrations, reaching pharmacologically active levels. The rise in ANF was negatively correlated with atrial pressures but positively correlated with atrial transmural pressures, atrial size, and calculated wall tension. Plasma ANF levels peaked at 515 +/- 95 pg/ml 40 minutes after relief of tamponade and leveled off at 140% to 180% of the pretap concentrations. Plasma cGMP exhibited a slightly delayed but similar time course to the rise in ANF levels, and urine flow rate increased fourfold in the 8 hours after relief of tamponade.(ABSTRACT TRUNCATED AT 250 WORDS)

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 myocardial infarction associated with intravenous injection of pentazocine and tripelennamine.

This case report describes the evolution of an acute anteroseptal myocardial infarction in a 27-year-old man following intravenous injection of pentazocine and tripelennamine. Subsequent coronary angiography showed normal coronary arteries. Based on the known mechanism of action of these drugs, it is postulated that myocardial infarction resulted from coronary artery spasm secondary to excessive catecholamine stimulation.

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.

Intercoronary connection and apical left ventricular hypertrophy: case report and review of the literature.

Cardiac catheterization in a 55-year-old man, presenting with chronic chest pain and new T wave inversion, showed apical left ventricular (LV) hypertrophy and a large intercoronary connection between the posterior descending artery (PDA) and left anterior descending (LAD). Although the LAD was normal, selective angiography of the right coronary artery (RCA) filled the LAD retrogradely. Possible mechanisms and the literature are reviewed.

Proximal aortic dissection with cardiac tamponade. Long-term survival without surgery.

Proximal aortic dissection in a 79-year-old woman was complicated by cardiac tamponade, aortic regurgitation, and pleural leak. Following pericardiocentesis and control of her hypertension, she survived without an operation for more than four years.

Origin and significance of diastolic Doppler flow signals in the left ventricular outflow tract.

Diastolic Doppler flow signals (greater than or equal to 0.2 m/s) in the left ventricular outflow tract have not been well characterized, and their origin and significance remain controversial. Fifty-nine patients (55 +/- 16 years of age) with technically good Doppler echocardiographic studies were studied prospectively. There were 14 normal subjects, 21 patients with left ventricular hypertrophy, 10 with dilated cardiomyopathy and 14 with other cardiac disease. The rhythm was sinus in 55 and atrial fibrillation in 4. Two distinct Doppler flow signals were detected in the left ventricular outflow tract during diastole. These were termed E' (early) and A' (active) because they occurred 40 to 100 ms after higher velocity mitral inflow E (passive filling) and A (atrial contraction) signals. Among 59 patients, E' signals were present in 48 (81%) and had a mean velocity of 0.41 +/- 0.23 m/s. In 55 patients with normal sinus rhythm, A' signals were present in 52 (95%) and had a mean velocity of 0.52 +/- 0.24 m/s. No A' signals were present in the four patients with atrial fibrillation. The E' and A' velocities by pulsed wave Doppler ultrasound were low at the left ventricular apex and increased along the basal septum in the left ventricular outflow tract. Prominent A' velocities (greater than or equal to 0.45 m/s) were seen in 62% of patients with left ventricular hypertrophy, 50% of normal subjects and 10% of patients with dilated cardiomyopathy. The A' velocity was higher in patients with left ventricular hypertrophy (0.63 +/- 0.26 m/s) than in those with a normal heart (0.45 +/- 0.16 m/s; p less than 0.05) or dilated cardiomyopathy (0.25 +/- 0.13 m/s; p less than 0.01). The major determinants of diastolic outflow tract velocity were the mitral inflow E and A velocities and left end-diastolic dimension, particularly when combined (r = 0.64, p less than 0.0001 for E'; r = 0.72, p less than 0.0001 for A'). Distinctive E' and A' Doppler outflow tract signals result from mitral inflow and may be detected in most patients with normal heart size. These E' and A' velocities increase from apex to base and are more prominent in patients with a small, normally contracting heart or left ventricular hypertrophy.

Long-term effects of excision of the mitral apparatus on global and regional ventricular function in humans.

To evaluate the long-term sequelae of mitral valve excision on global and regional wall motion, contrast left ventriculograms from 21 patients with suspected prosthetic mitral valve dysfunction performed 10.4 +/- 2.1 years after mitral valve replacement were analyzed by a computerized radial shortening method. Patients with significant coronary artery disease (greater than 30% stenosis in any vessel) were excluded. In 8 of the 21 patients in whom preoperative ventriculograms were available, regional wall motion was normal before valve replacement. Although average radial shortening (35.6 +/- 4.8% versus 35.3 +/- 3.8%, p = NS) and left ventricular ejection fraction (62.8 +/- 4.2% versus 57.9 +/- 2.8%, p = NS) were unchanged in the preoperative and postoperative studies of these eight patients, radial shortening in the vicinity of insertion of the posteromedial papillary muscle declined significantly (38.4 +/- 6.4% to 20.8 +/- 4.4%, p less than 0.04). Postoperative radial shortening for all 21 patients at the site of insertion of the papillary muscle was also reduced to a significant degree compared with the average radial shortening (32.9 +/- 10.3% versus 17.5 +/- 2.0%, p less than 0.001). The findings demonstrate significant long-term and possibly permanent regional ventricular dysfunction after severing the chordae tendineae during mitral valve replacement.