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M Shahi

Publications and source records attributed to M Shahi.

At least 37 records · Page 2Linked to original sources

Transesophageal dobutamine-atropine stress echocardiography: diagnostic accuracy for coronary stenosis detection and localization.

Transesophageal echocardiography with dobutamine-atropine stress (TE-DASE) is a recently described technique for evaluation of coronary artery disease (CAD). We undertook this study prospectively to determine the feasibility, reliability and safety of this procedure in patients with known CAD and to evaluate its diagnostic accuracy for coronary stenoses of varying severity. Thirty-seven patients who underwent coronary arteriography (CART) and TE-DASE within a 3-month interval without intervening ischemic events or revascularisation were included in the study CART and stress echograms were independently evaluated by different observers. Stenosis was measured with calipers and a > or = 50% lumen diameter stenosis was considered significant. A reduction or lack of endocardial motion and/or wall thickening on progressive incremental stress was considered an abnormal response. TE-DASE could be successfully completed in 33/37 (90%) patients. Using a modified 16-segment model of the left ventricle (LV), 15.2 +/- 0.8 segments/patient and 501/528 (95%) segments overall could be optimally evaluated. Inter-observer concordance for an abnormal response was 94%. Predictive accuracies for one-vessel disease (1-VD), two-vessel disease (2-VD) and three-vessel disease (3-VD) were 88, 58 and 23% respectively. Overall sensitivity for detection of a significant (> or = 50%) stenosis was 72% (32% for moderate (50-69%), 90% for severe (> or = 70%) stenosis) and specificity was 96%. Diagnostic accuracy for localisation of significant stenosis was 95% for the left anterior descending artery (LAD), 86% for the left circumflex artery (LCX) and 88% for the right coronary artery (RCA). There were no major complications. We conclude that TE-DASE is a safe, reliable and easily-performed procedure and provides excellent visualisation of myocardial segments. Diagnostic accuracy for detection of severe stenosis and its localisation is excellent.

Atropine↗

Left ventricular hypertrophy and QT dispersion in hypertension.

The interlead variation in QT length on a standard electrocardiograph reflects regional repolarization differences in the heart. To investigate the association between this interlead variation (QT dispersion) and left ventricular hypertrophy, we subjected 100 untreated subjects to 12-lead electrocardiography and echocardiography. Additionally, 24 previously untreated subjects underwent a 6-month treatment study with ramipril and felodipine. In the cross-sectional part of the study, QT dispersion corrected for heart rate (QTc dispersion) was significantly correlated with left ventricular mass index (r = .30, P < .01), systolic pressure (r = .30, P < .01), the ratio of peak flow velocity of the early filling wave to peak flow velocity of the atrial wave (E/A ratio) (r = -.22, P = .02), isovolumic relaxation time (r = .31, P < .01), and age (r = .21, P < .04). In the treatment part of the study, lead-adjusted QTc dispersion decreased from 24 to 19 milliseconds after treatment, and after a subsequent 2 weeks of drug washout remained at 19 milliseconds (P < .01). The changes in left ventricular mass index at these stages were 144, 121, and 124 g/m2 (P < .01). Systolic pressure decreased from 175 to 144 mm Hg and increased again to 164 mm Hg after drug washout (P < .01). The E/A ratio (0.97, 1.02, and 1.02; P = 69) and isovolumic relaxation time (111, 112, and 112; P = .97) remained unchanged through the three assessment points. In conclusion, QT dispersion is increased in association with an increased left ventricular mass index in hypertensive individuals. Antihypertensive therapy with ramipril and felodipine reduced both parameters. If an increased QT dispersion is a predictor of sudden death in this group of individuals, then the importance of its reduction is evident.

Adult↗

Left ventricular diastolic function in hypertension: a 4 year follow-up study.

In order to assess the long term effects of antihypertensive treatment on left ventricular diastolic function, 26 hypertensive patients were followed up for a mean of 4.25 years with two-dimensional and Doppler echocardiography. A significant reduction in left ventricular mass index was first apparent after 9 months of therapy (mean (S.D.) 124 (22) vs. 114 (18) g/m2, P < 0.01), and this was maintained over the 4.25 year period (124 (22) vs. 117 (17) g/m2, p < 0.05). At 9 months there was no change in either isovolumic relaxation time (108 (26) vs. 108 (17) ms, P = N.S.) or left ventricular filling as assessed by peak flow velocity E/A ratio (0.94 (0.22) vs. 0.95 (0.27), P = N.S.). However, after 4.25 years there was a significant improvement in IVRT (108 (26) vs. 83 (11) ms, P < 0.01) with a trend towards an improved peak flow velocity E/A ratio, although this did not reach statistical significance (0.95 (0.27) vs. 1.02 (0.26), P = N.S.). Of the 14 patients who had an abnormal isovolumic relaxation time at baseline, 12 normalised and 2 improved. These findings suggest that left ventricular diastolic dysfunction in hypertension may be reversed by prolonged antihypertensive treatment.

Adult↗

Replacement treatment with biosynthetic human growth hormone in growth hormone-deficient hypopituitary adults.

OBJECTIVES: The physiological role of growth hormone in adult life has recently attracted increased interest. We have studied the clinical effects and the effects on body composition of prolonged replacement with biosynthetic human GH in a large number of hypopituitary adults. DESIGN: A randomized double blind placebo controlled trial for 6 months followed by an open trial of GH treatment for 12 months. GH daily dose was 0.04 (0.02-0.05) IU/kg s.c. PATIENTS: Forty GH deficient hypopituitary patients (19 M, 21 F; aged 19-67 years) on conventional replacement therapy were studied. MEASUREMENTS: Serum insulin like growth factor I (IGF-I), skinfold thickness, total body potassium, total body water (TBW), exercise tolerance and muscle strength, and well-being. RESULTS: During the 6-month double blind phase, two GH treated patients withdrew because of adverse events. Lean body mass (LBM) increased and percentage body fat (%BF) decreased on GH but not on placebo (P) (LBM: (GH: from 48.5 +/- 9.6 to 49.6 +/- 9.5 kg; P: from 50.9 +/- 9.2 to 50.1 +/- 9.0 kg, P < 0.05 GH vs P) and %BF (GH: from 34.7 +/- 11.4 to 34.2 +/- 10.7; P: from 37.4 +/- 7.6 to 38.7 +/- 8.1, P < 0.05 GH vs P)). TBW increased on GH (P < 0.01) but not on P. No change was observed in waist-to-hip ratio or in muscle strength. During longer-term follow-up combining the double blind and open phase components of the study, 34, 27 and 11 patients received GH for 6, 12 and 18 months respectively. Patients dropped out because of adverse events or lack of perceived benefit. Skinfold thicknesses decreased significantly at 6 and 12 months and the waist circumference at 6 months. Waist-to-hip ratio decreased significantly on GH at 12 months. LBM increased on GH treatment from 49.6 +/- 9.1 to 51.6 +/- 9.4 kg (P < 0.0006), 51.9 +/- 8.9 kg (P < 0.07) and 53.1 +/- 10.5 kg (P < 0.0001) at 6, 12 and 18 months respectively. Percentage body fat decreased on GH from 37.2 +/- 10.7 to 34.7 +/- 10.1 (P < 0.005), 35.1 +/- 12.8 (NS) and 34.5 +/- 8.6 (P < 0.04) at 6,12 and 18 months respectively. TBW also increased at 6 and 12 months of GH treatment. Exercise time increased significantly at 6, 12 and 18 months of GH treatment. Muscle strength in selected muscle groups increased significantly at 6, 12 or 18 months of GH treatment. Randomization resulted in the placebo group having a greater GHQ score (higher morbidity) than the GH group before therapy. Over the controlled phase, GHQ scores improved on placebo but not on GH and CPRS score was unchanged in either group. In the open phase, the GHQ score did not change on GH therapy but CPRS score improved at 6 and 12 months. CONCLUSIONS: Growth hormone replacement therapy in adults for 6 months increased lean body mass, total body water and exercise tolerance, and decreased body fat. Growth hormone replacement for longer than 6 months maintains the advantageous effects seen in shorter-term studies and may have additional effects on body fat distribution, muscle strength and psychological well-being.

Adult↗

Cardiovascular effects of prolonged growth hormone replacement in adults.

OBJECTIVES: To study the cardiovascular effects of human growth hormone (GH) replacement therapy in adults. INTERVENTION: Biosynthetic human GH given in a daily dose of 0.04 +/- 0.01 IU kg-1 for 6-18 months in an open trial. PATIENTS: Thirty-four GH-deficient hypopituitary patients on conventional replacement therapy, aged 19-67 years and with a body mass index of 18.0-410.0 kg/m2. MEASUREMENTS: Resting blood pressure, exercise tolerance, renal function and routine blood counts were assessed every 6 months. Two-dimensional echocardiography and Doppler ultrasound scanning were performed at 0, 6 and 12 months of GH therapy. RESULTS: Exercise time increased significantly on GH from 9.37 +/- 2.64 min at the start to 10.39 +/- 2.86 min (P < 0.001), 10.90 +/- 2.48 min (P < 0.001) and 11.11 +/- 0.70 min (P < 0.001) at 6, 12 and 18 months respectively. There was no change in the heart rate or in the blood pressure at rest nor at the peak of exercise. No significant changes were observed in measures of cardiac structure (left ventricular mass index, left ventricular posterior wall thickness and interventricular septal thickness), ejection fraction nor in cardiac output. Isovolumic relaxation time, a marker of diastolic function, decreased in 24 patients after 6 months on GH (from 98.6 +/- 15.9 to 89.6 +/- 15.2 ms; P < 0.03) but it was not different from baseline in the 18 patients who were restudied at 12 months. There was no significant change in the left ventricular filling neither at 6 nor at 12 months. No significant, changes were observed in plasma electrolytes, creatinine nor in blood count on GH treatment. CONCLUSIONS: Growth hormone replacement therapy in hypopituitary adults for 6-18 months produced sustained increase in exercise tolerance but was not associated with changes in cardiac structure or systolic function.

Adult↗

Plasma mediated neutrophil stimulation during coronary angioplasty: autocrine effect of platelet activating factor.

BACKGROUND: Polymorphonuclear neutrophils are involved in the development of myocardial injury during ischaemia and reperfusion. Coronary angioplasty has been shown to result in neutrophil activation. This may be a result of contact with ligands expressed by endothelial cells or response to soluble stimuli released from ischaemic tissue into the plasma or both. OBJECTIVE: To investigate plasma mediated neutrophil activation during angioplasty. METHODS AND RESULTS: Plasma samples were collected from the coronary sinus, femoral artery, and femoral vein of 14 patients undergoing angioplasty, before and after the first balloon inflation and at the end of the procedure. Plasma samples were incubated with washed neutrophils isolated from healthy donors. Expression of the adhesion molecules CD18 integrin and L-selectin (Leu-8) was measured by flow cytometry, and superoxide anion production was measured by chemiluminescence. Plasma samples from the coronary sinus and femoral artery but not from the peripheral vein induced increased expression of neutrophil CD18 after balloon deflation. Modification of the expression of L-selectin was not noted. Production of superoxide anion by neutrophils was stimulated by plasma samples from the coronary sinus, but not by those from the femoral artery or vein. This plasma mediated neutrophil stimulation was prevented when the neutrophils were pretreated with platelet activating factor receptor antagonists BN52021 or BN50739. The platelet activating factor concentration detected in the coronary sinus was not higher than in control plasma. CONCLUSION: Brief ischaemia during coronary angioplasty leads to the release of soluble stimuli capable of inducing neutrophil integrin expression and free oxygen radical production. Platelet activating factor may act as an autocrine neutrophil stimulus under these conditions.

Angioplasty, Balloon, Coronary↗

Structural changes in the cardiovascular system of untreated essential hypertensives.

Arterial hypertension is associated with structural changes in the cardiovascular system. This study has examined the effect of hypertension on the carotid artery wall and examined the relation between changes in the structure of carotid artery wall and left ventricle in untreated hypertensives. The carotid artery wall was visualized using a high resolution ultrasound technique in 37 untreated hypertensive patients (25 males, 12 females) and 37 age and sex matched normotensive individuals and carotid intima-media thickness (IMT) and carotid artery diameter measured. IMT and intima-media cross sectional area was significantly greater in the hypertensive group compared with the normotensive group, though the carotid artery diameter did not differ significantly. There was a significant association between age and IMT in both groups. In the hypertensive group there was also a significant association between left ventricular mass index, ventricular septal or posterior wall thickness and IMT. This study indicates that there is an association between cardiac and carotid arterial structure in hypertension. Such a relationship may be important in understanding the associated risks of high blood pressure.

Adult↗

The effects of antihypertensive therapy on carotid vascular structure in man.

OBJECTIVE: An increased carotid intima-media thickness (IMT) has been found to be associated with a number of cardiovascular risk factors such as age, hypertension, cigarette smoking, hypercholesterolaemia and left ventricular hypertrophy. Our objective was to assess whether carotid intima-media thickness in hypertensive patients could be reduced by antihypertensive therapy. METHODS: 13 hypertensive patients, 10 previously untreated, were examined using carotid ultrasonography and echocardiography at baseline and then at 8 weeks and 39 weeks after commencement of antihypertensive therapy with ramipril and the second-line addition of felodipine. RESULTS: By the end of the study significant regression of IMT (0.1(0.05-0.16) mm, F-value 10.2, P < 0.01) and left ventricular mass index had occurred (25(10.7-39.3) g/m2, F-value 9.7, P < 0.01). The reduction in IMT was significantly related to the reduction in mean arterial pressure, r = 0.55, P = 0.05). CONCLUSION: Antihypertensive therapy with ramipril and felodipine causes regression of IMT in hypertensive patients, probably chiefly through blood pressure reduction. Large prospective studies are required to assess whether a reduction in IMT results in a reduction in morbidity and mortality.

Adult↗

Left ventricular structure and function in previously untreated hypertensive patients: the importance of blood pressure, the nocturnal blood pressure dip and heart rate.

BACKGROUND: Cardiac assessment is an important part of risk stratification in hypertensive patients. Left ventricular hypertrophy in particular is a powerful predictor of subsequent cardiovascular morbidity and mortality. Previous studies assessing haemodynamic factors that may be responsible for cardiac changes in hypertensive patients have been performed in those previously treated for hypertension. To investigate more fully these haemodynamic relationships, a large group of previously untreated patients were studied. METHODS: Ninety-eight previously untreated hypertensive patients underwent electrocardiography, two-dimensional and Doppler echocardiography, 24 h ambulatory blood pressure monitoring and exercise stress testing. RESULTS: The left ventricular mass index (LVMI) was more closely related to mean 24 h than to clinic blood pressures (24 h systolic r = 0.48, P < 0.01; 24 h diastolic r = 0.49, P < 0.01; clinic systolic r = 0.28, P < 0.01; clinic diastolic r = 0.31, P < 0.01). In addition, the systolic nocturnal blood pressure dip was found to be inversely related to LVMI in men (r = -0.32, P < 0.01). Of the indices of left ventricular diastolic function, age (r = -0.64, P < 0.01), heart rate (r = -0.25, P = 0.02) and LVMI (r = -0.22, P = 0.02) were independently related to the E-A ratio. Age (r = 0.40, P < 0.01), blood pressure (systolic r = 0.39, P < 0.01; diastolic r = 0.43, P < 0.01), the nocturnal blood pressure dip (systolic r = -0.38, P < 0.01, diastolic r = -0.31, P < 0.01) and LVMI (r = 0.37, P < 0.01) were independently related to the isovolumic relaxation time. CONCLUSIONS: Blood pressure was the only independent determinant of LVMI; nocturnal blood pressure may be particularly important in men. Age and both haemodynamic and structural factors are independent determinants of parameters of left ventricular diastolic function in hypertensive patients.

Blood Pressure↗

Ventricular arrhythmias in hypertension: in which patients do they occur?

OBJECTIVE: It has been suggested that the increased incidence of sudden death in hypertensive patients, particularly those with left ventricular hypertrophy, may be casually related to the increased number and complexity of ventricular arrhythmias that have been demonstrated in these patients. The objective of the present study was to assess some of the factors which might be responsible for these arrhythmias. SUBJECTS AND METHODS: One hundred and three untreated subjects were divided into four groups on the basis of blood pressure and echocardiographic measurements: hypertensive patients with left ventricular hypertrophy (n = 38), hypertensive patients without left ventricular hypertrophy (n = 16), patients with borderline or white-coat hypertension (n = 26) and normotensive subjects (n = 23). Each subject underwent two-dimensional and Doppler echocardiography, 12-lead electrocardiogram examination, 12-lead electrocardiogram exercise stress testing, 24-h ambulatory blood pressure monitoring and 24-h Holter monitoring. A further 17 hypertensive patients with left ventricular hypertrophy who were on long-term antihypertensive therapy were also investigated in the same manner and compared with untreated hypertensive patients with left ventricular hypertrophy who were matched for age, sex and race. RESULTS: Untreated hypertensive patients, even with left ventricular hypertrophy, had a low prevalence of frequent or complex arrhythmias (seven out of 80 patients with Lown score 2+). In contrast, hypertensive patients with left ventricular hypertrophy on long-term antihypertensive therapy had a significantly greater prevalence of complex arrhythmias than untreated patients with left ventricular hypertrophy (eight out of 17 treated patients compared with two out of 17 untreated patients with Lown score 2+). CONCLUSIONS: Hypertensive patients with left ventricular hypertrophy who had received long-term antihypertensive therapy were found to have a high prevalence of complex ventricular arrhythmias, which was in contrast to untreated hypertensive patients, even those with left ventricular hypertrophy. This may reflect the consequences on the left ventricle of long-term antihypertensive treatment. If complex ventricular arrhythmias are implicated in the excess of sudden deaths in hypertensive patients, this might be an important factor.

Adult↗

Racial differences in cardiac structure and function in essential hypertension.

OBJECTIVE: To assess racial differences in cardiac structure and function in patients presenting with previously untreated hypertension. DESIGN: Untreated black patients with hypertension were compared with untreated white patients matched for age and sex. Both groups had similar body mass indices, blood pressures, and reported duration of hypertension. SETTING: Cardiovascular risk factor clinic for outpatients. SUBJECTS: 36 men and 22 women with untreated essential hypertension. MAIN OUTCOME MEASURES: Variables of heart structure and function on cross sectional and Doppler echocardiography. RESULTS: The black patients had a significantly greater interventricular septal thickness (mean 1.23 (95% confidence interval 1.14 to 1.33) v 1.09 (1.02 to 1.16) cm; P = 0.02) and posterior wall thickness (mean 1.14 (1.07 to 1.22) v 0.96 (0.88 to 1.03) cm; P = 0.001) than the white patients, although left ventricular internal diameter was not significantly different (mean 4.90 (4.68 to 5.12) v 4.82 (4.64 to 5.01) cm; P = 0.59). This resulted in a significantly greater left ventricular mass index (mean 151 (137 to 164) v 120 (107 to 133) g/m2; P = 0.001) and relative wall thickness (mean 0.47 (0.43 to 0.51) v 0.40 (0.37 to 0.42) cm; P = 0.004) in the black patients. Comparison of Doppler measures of left ventricular diastolic function showed a significantly longer isovolumic relaxation time in black patients (mean 107 (98 to 116) v 92 (83 to 101) ms; P = 0.02) compared with white patients, although peak early to atrial filling ratios were similar in both groups (mean 1.14 (0.95 to 1.32) v 1.04 (0.94 to 1.15); P = 0.37). CONCLUSION: Among previously untreated hypertensive patients, black subjects compared with white subjects have significantly higher left ventricular mass index and relative wall thickness, as well as more impairment of left ventricular function during diastole.

Adult↗

Cardiovascular effects of growth hormone replacement therapy in hypopituitary adults.

In the present study the effects of replacement with biosynthetic human growth hormone (GH) in a large group of hypopituitary adults on cardiac structure and function were investigated. Thirty-six GH-deficient, hypopituitary patients (17 males and 19 females; aged 19-67 years) on conventional replacement therapy without GH were studied. Twenty-nine of the patients had acquired hypopituitarism in adult life, mainly due to pituitary tumours. The design of the study was a prospective, randomized, double-blind placebo-controlled trial for 6 months. Growth hormone (17 patients) was given in a daily dose of 0.02-0.05 IU/kg body wt sc (or a placebo, 19 patients) according to the patients' tolerance. Other pituitary replacement treatment was unchanged. Resting and exercise electrocardiography using the Bruce protocol, two-dimensional echocardiography, Doppler ultrasound scanning and serum insulin-like growth factor I (IGF-I) were assessed at 0 and 6 months. Resting blood pressure was measured at 0, 1, 3 and 6 months. Serum IGF-I increased significantly on GH treatment (mean +/- SD) GH: 293 +/- 197 vs placebo: 82 +/- 40 micrograms/l; p < 0.0001 at 6 months). Exercise time increased significantly on GH but not on placebo (GH: 8.45 +/- 3.16 to 9.38 +/- 2.42 min.sec, p < 0.01; placebo 9.08 +/- 4.35 to 9.50 +/- 4.14 min.sec, NS), although the change was not significantly different between the two. There was no change in the heart rate or the blood pressure either at rest or at the peak of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Structural changes in the heart and carotid arteries associated with hypertension in humans.

Hypertension is associated with structural changes in the vascular system and in the heart. This study has examined the relationships between carotid artery intima-media thickness and other risk factors in 52 untreated patients (20 hypertensive). Carotid intima-media thickness was measured bilaterally using a Duplex doppler ultrasonic scanner. In the hypertensive individuals the left ventricle was examined by echo-cardiography and the left ventricular mass index determined. There was a significant association between age and IMT, and both SBP and DBP and IMT. The IMT in the hypertensive group was significantly larger than in the normotensive group and in the hypertensive subjects there was a positive association between left ventricular mass index and IMT. There was no significant difference in calculated media stress between the normotensive and hypertensive groups, probably due to a small increase in carotid intima-media area combined with a small reduction in carotid lumen diameter. Hypertension is associated with a thickening of the intima-media of the carotid artery and an increase in left ventricular mass. Whether these changes in cardiac and arterial structure are in response to similar influences remains to be established.

Adolescent↗

Effectiveness and safety of a single intravenous bolus injection of tissue-type plasminogen activator in acute myocardial infarction. Bolus Dose-Escalation Study of Tissue-Type Plasminogen Activator (BEST) Investigators.

The efficacy of multiple intravenous bolus injections of tissue-type plasminogen activator (t-PA) in inducing rapid coronary recanalization in patients with acute myocardial infarction was previously demonstrated. In this Bolus Dose-Escalation Study of Tissue-Type Plasminogen Activator (BEST), the efficacy of 3 different doses of a single rapid intravenous bolus injection of t-PA (dute-plase, Wellcome Foundation, London) in inducing coronary patency (Thrombolysis In Myocardial Infarction perfusion grade 2 or 3) in 64 patients with acute myocardial infarction presenting less than 6 hours after onset of symptoms was investigated. At 60 minutes after administration of t-PA, the infarct-related coronary artery was patent in 9 of 17 patients (53%; 95% confidence interval [CI] 28 to 77%) after 0.3 MU/kg, in 14 of 23 (61%; 95% CI 39 to 80%) after 0.45 MU/kg and in 10 of 14 (71%; 95% CI 42 to 92%) after 0.6 MU/kg. At 90 minutes after t-PA, coronary patency was present in 9 of 17 cases (53%; 95% CI 28 to 77%) after 0.3 MU/kg, in 12 of 24 (50%; 95% CI 29 to 71%) after 0.45 MU/kg and in 10 of 13 (77%; 95% CI 46 to 95%) after 0.6 MU/kg. One patient in each dose group had a silent reoccluded infarct-related artery by 24 hours, and there were 2 clinical reinfarctions before discharge. No major bleeding events were observed. There were 5 hospital deaths, all unrelated to t-PA. A single intravenous bolus injection of 0.6 MU/kg of t-PA appears to be effective in inducing rapid coronary patency and to be safe in patients with acute myocardial infarction.

Adult↗

Myocardial dysfunction in treated adult hypopituitarism: a possible explanation for increased cardiovascular mortality.

OBJECTIVE: To assess cardiac structure and function in patients with treated hypopituitarism and to determine their relation to the degree of growth hormone deficiency and body composition pattern. DESIGN: 26 patients with treated hypopituitarism were studied by cross sectional and Doppler echocardiography and by exercise testing. The results were analysed and their relation to the degree of growth hormone deficiency and body composition determined. SETTING: All tests were performed in the department of cardiology and the unit of metabolic medicine at a tertiary referral centre. PATIENTS: Patients with hypopituitarism referred for endocrine assessment. MAIN OUTCOME MEASURES: Left ventricular mass, left ventricular diastolic function, and exercise capacity in patients with hypopituitarism and their relation to growth hormone deficiency. RESULTS: Mean (SD) serum concentration of insulin-like growth factor 1 (IGE-1), a measure of growth hormone deficiency, was 82.4 (45) micrograms/l. Lean body mass calculated by measuring total body potassium was 50 (9) kg. All patients had a normal left ventricular mass index and a normal left ventricular ejection fraction. Eight patients had abnormal left ventricular diastolic function. There was a significant correlation between IGF-1 and left ventricular mass (r = 0.45, p less than 0.02). Lean body mass was also significantly correlated with left ventricular mass (r = 0.78, p less than 0.0001) and left ventricular diastolic function (r = -0.63, p less than 0.01). The mean exercise duration was 8.6 (3.6) minutes. There was a significant correlation between serum IGF-1 and the rate-pressure product on exercise (r = 0.47, p less than 0.01). Seven patients had planar ST segment depression greater than 0.1 mV during exercise testing. In five of these patients there was rapid resolution of ST segment depression immediately after exercise. Two patients developed considerable ST segment depression, and subsequent coronary angiography showed normal coronary arteries. Exercise-induced ST segment depression was not related to the severity or duration of growth hormone deficiency or serum cholesterol concentration. CONCLUSIONS: This study suggests that left ventricular mass and the rate-pressure product are related to the degree of growth hormone deficiency, that left ventricular diastolic dysfunction is frequently seen in hypopituitarism, and that these patients may have ischaemic-like ST segment changes during exercise testing. These findings may explain the increased cardiovascular mortality in patients with hypopituitarism and may also have implications for growth hormone replacement therapy in adults.

Adult↗

Metabolic changes and vascular risk factors in hypopituitarism.

Adults with hypopituitarism die prematurely, and the excess mortality is from vascular disease. On echocardiography we have demonstrated abnormalities of myocardial diastolic function in hypopituitary adults, indicating possible early ischaemic change. Peripheral arterial disease is evident on ultrasonography. Vascular risk factors have also been examined. Impaired glucose tolerance and unrecognized diabetes are common in hypopituitary adults. Total cholesterol levels are elevated, particularly in hypopituitary women. The role of growth hormone (GH) deficiency in the vascular disease and in the vascular-risk-factor abnormalities is unknown at present. Prolonged GH therapy causes a decrease in the levels of fasting total cholesterol, without any adverse effects on glucose homeostasis. GH therapy trials in adults will clarify the role of GH in the excess vascular risk of hypopituitarism. Prolonged GH therapy will be necessary for the vascular effects to be defined.

Adult↗

Impaired left ventricular filling during ST-segment depression provoked by dipyridamole infusion in patients with syndrome X.

The left ventricular filling and regional wall motion patterns were compared in 6 normal subjects, 20 patients with coronary artery disease, and 10 patients with syndrome X by means of Doppler and two-dimensional echocardiography during high-dose (0.9 mg/kg body weight in 10 min) dipyridamole infusion. During the procedure none of the normal subjects had chest pain or significant ST depression (greater than 0.1 mV) whereas 10 of 20 patients with coronary artery disease had ST depression, 3 with chest pain. Six patients with syndrome X had ST depression, 5 with chest pain. Regional wall motion abnormalities were identified in 6 patients with coronary artery disease who had ST depression but none were detected in normals or in patients with syndrome X. Compared with normals (-2.1 +/- 3.5%) there was a significant difference in percentage decrease in the peak early filling velocity in patients with coronary artery disease and ST depression (-10.3 +/- 6.2%; p less than 0.01) and in patients with syndrome X and ST depression (-9.4 +/- 6.9%; p less than 0.05). These findings indicate that, in the presence of dipyridamole-induced ST depression, patients with syndrome X have an abnormal left ventricular filling pattern similar to that observed in patients with coronary artery disease. This suggests that myocardial ischemia occurs in patients with syndrome X but the absence of regional wall motion abnormality suggests that it is diffuse.

Aged↗

The effects of blood pressure reduction on abnormal left ventricular diastolic function in hypertensive patients.

To investigate whether reduction in blood pressure has a beneficial effect on left ventricular diastolic function, we investigated 20 hypertensive patients with evidence of diastolic dysfunction at baseline and at 3 and 6 months after initiation of captopril therapy. Two-dimensional echocardiography was used to determine left ventricular mass index and Doppler ultrasound to assess diastolic function. Fifteen of the 20 patients had a significant reduction in blood pressure at 3 and 6 months and left ventricular mass index remained unchanged during the study period. Despite reduction in blood pressure, no difference in isovolumic relaxation time, early and atrial filling velocities or their ratio was observed. Our results suggest that a direct relationship between blood pressure and left ventricular diastolic function does not exist and that other factors such as alterations in muscle or collagen composition of the left ventricle may be more important in determining abnormal diastolic function in hypertension.

Adult↗