An evaluation of nasal patency with acoustic rhinometry--preop. and postop. comparisons

PURPOSE: This prospective study was designed to assess the effect of primary hyperparathyroidism on heart muscle, valves, and myocardial function. Echocardiography was used to evaluate changes in mechanical performance, the thickness of the left ventricular wall, myocardial calcific deposits, and valvular calcifications in patients with primary hyperparathyroidism. METHODS: Echocardiography was performed in 54 patients with hyperparathyroidism prior to surgery and 12 +/- 2 months after successful parathyroidectomy. A matched control group was followed for comparison. RESULTS: In a blinded fashion, aortic and mitral valve calcifications were detected in 63% and 49% of patients with primary hyperparathyroidism (controls: 12% and 15%, respectively). Calcific deposits in the myocardium were found in 69% of patients with hyperparathyroidism and 17% of the control subjects. After parathyroidectomy and 12 months of normocalcemia, a significant regression of left ventricular hypertrophy (p < 0.001) was observed. CONCLUSIONS: The present data show a high incidence of left ventricular hypertrophy, calcific deposits in the myocardium, and/or aortic and mitral valve calcification in patients with primary hyperparathyroidism. A 1-year follow-up after parathyroidectomy (and restoration of normocalcemia) discloses regression of hypertrophy, while calcifications persist without evidence of progression.     

Intracellular calcium and blood pressure: comparison between primary hyperparathyroidism and essential hypertension

Intracellular calcium has been reported to be increased in essential hypertension, and thought to play a role in its genesis through facilitation of vascular smooth muscle contraction. Since hypertension is more prevalent in primary hyperparathyroidism, intracellular calcium may also be increased in this condition. To investigate whether the hyperparathyroid condition, i.e., hypercalcemia and increased PTH per se, could be associated with high intracellular calcium, we measured intracellular calcium in platelets with the Quin-2 AM fluorometric method in 11 normotensive patients with primary hyperparathyroidism, 15 patients with essential hypertension, and 18 normal controls, all matched for age and sex. We repeated the measurements in 9 of the hyperparathyroid patients after successful surgery. We found that intracellular calcium was higher in normotensive patients with primary hyperparathyroidism than in normal controls (198 +/- 24 vs 113 +/- 11 nM, p < 0.05), but lower than in patients with essential hypertension (198 +/- 24 vs 286 +/- 38 nM, p < 0.05). Successful removal of a parathyroid adenoma decreased intracellular calcium from 215 +/- 22 to 116 +/- 19 nM, (p < 0.01). In the patients with primary hyperparathyroidism, intracellular calcium was strongly correlated with the levels of PTH (r = 0.87, p < 0.01), but not with the total serum calcium levels (r = 0.04, NS). The decrease in intracellular calcium after parathyroidectomy was also strongly correlated with the decrease in PTH (r = 0.84, P < 0.01), but not with the decrease in total serum calcium (r = 0.16, NS). In the patients with essential hypertension, intracellular calcium correlated well with systolic (r = 0.69, p < 0.01), diastolic (r = 0.76, p < 0.01) and especially mean arterial pressure (r = 0.86, P < 0.01). There was no correlation between blood pressure and intracellular calcium in the patients with primary hyperparathyroidism. We conclude that normotensive patients with primary hyperparathyroidism, as well as patients with essential hypertension, can have increased concentrations of intracellular calcium in platelets. The correction of the hyperparathyroid condition normalizes intracellular calcium concentration. The close correlation between PTH and intracellular calcium suggests that PTH may act as a ionophore for calcium entry into cells. Whether the increased levels of intracellular calcium may reflect a pre-hypertensive condition in normotensive patients with primary hyperparathyroidism remains to be determined.     

Determinants of the pulmonary artery pressure rise in left ventricular dysfunction

Pulmonary artery hypertension in patients with left ventricular dysfunction is related to poor outcome but the role of cardiac functional abnormalities in the genesis of pulmonary hypertension remains unknown. The aim of this prospective study was to identify the determinants of pulmonary hypertension in 102 consecutive patients with primary left ventricular dysfunction (ejection fraction < 50%). Systolic pulmonary artery pressure was measured by continuous wave Doppler. Left ventricular systolic and diastolic function, severity of functional mitral regurgitation, cardiac output, and left atrial volume were assessed using Doppler echocardiography. In patients with left ventricular dysfunction, systolic pulmonary artery pressure was increased (51 +/- 14 mmHg, range 23 to 87 mmHg). Mitral deceleration time (r = -0.61; p = 0.0001) and mitral effective regurgitant orifice (r = 0.50; p = 0.0001) were the strongest parameters related to systolic pulmonary artery pressure. Multivariate analysis identified these two variables as the strongest predictors of systolic pulmonary artery pressure in association with the mitral E/A ratio (p = 0.006) and age (p = 0.005). In conclusion, pulmonary hypertension is common and variable in patients with left ventricular dysfunction. It is closely related to diastolic dysfunction and severity of functional mitral regurgitation but not independently to the degree of left ventricular systolic dysfunction. These findings underline the importance of assessing diastolic function and quantifying mitral regurgitation in patients with left ventricular dysfunction.     

Effects of antihypertensive therapy on left atrial function

OBJECTIVES: To investigate left atrial (LA) function as a reservoir, as a conduit and as a booster pump in essential hypertension (EH). LA volumes were echocardiographically measured in 28 untreated hypertensive patients and in 20 control subjects. BACKGROUND: LA makes a large contribution in left ventricular filling, especially in patients with impaired diastolic function. LA function is fundamental in left ventricular filling in hypertensive patients as hypertension results in left ventricular diastolic dysfunction. METHODS: Diagnosis of EH (blood pressure > 140/90 mm Hg) was based on three repeated readings of blood pressure (BP). Patients with myocardial infarction, cardiomyopathy, valvular or congenital heart disease were excluded. Doppler diastolic early (E) and late (A) velocity of mitral inflow were measured. The following indexes were calculated: left ventricular mass index (LVMI) using the Penn convention; left ventricular stroke volume (LVSV); LA reservoir volume (LARV = LA maximal volume at mitral valve opening minus minimal volume); LA conduit volume (LACV = LVSV-LARV). Atrial systolic function was assessed by calculating the active emptying fraction (volume at onset of atrial systole minus minimal volume/volume at onset of atrial systole, the E/A ratio and the LA ejection force (0.5 rho A2 MOA, where rho = the density of blood, MOA = mitral orifice area from the parasternal short axis view). Measurements were obtained in all hypertensive patients before and after 16 weeks administration of either enalapril (10 or 20 mg) or enalapril +/- chlorthalidone (20/25 mg) once a day. RESULTS: After 16 weeks of treatment, BP was reduced significantly (from 172/110 to 137/86 mm Hg, P < 0.001). LVMI decreased significantly as well (from 141 to 123 g/m2) although it was higher compared to controls (94 g/m2, P < 0.001). LARV decreased significantly (from 35.4 to 29.3 cm3, P < 0.05) while LACV increased significantly (from 43.8 to 51.3 cm3, P < 0.05), LA active emptying fraction and E/A ratio did not change. LA ejection force decreased significantly (from 20.9 to 18.1 kdynes, P < 0.05) but it was greater than controls (16.7 kdynes, P < 0.01). There was a positive relationship of LVMI to LARV (P < 0.01) in controls (r = 0.77) which held true in hypertensive patients, before (r = 0.72) and after treatment (r = 0.69). There was a negative relationship of LVMI to LACV (P < 0.01) in controls (r = -0.65), and in hypertensive patients untreated (r = -0.74) and after treatment (r = -0.72). CONCLUSIONS: Our results showed that in hypertensive patients, LA reservoir function increases and LA conduit function decreases, while LA ejection force increases. Antihypertensive treatment with enalapril and/or thiazide, induces normalisation of the LA function in parallel to left ventricular hypertrophy regression.     

Stress-induced left ventricular outflow tract obstruction: a potential cause of dyspnea in the elderly

OBJECTIVES: We sought to identify the pattern of disturbed left ventricular physiology associated with symptom development in elderly patients with effort-induced breathlessness. BACKGROUND: Limitation of exercise tolerance by dyspnea is common in the elderly and has been ascribed to diastolic dysfunction when left ventricular cavity size and systolic function appear normal. METHODS: Dobutamine stress echocardiography was used in 30 patients (mean [+/-SD] age 70 +/- 12 years; 21 women, 9 men) with exertional dyspnea and negative exercise test results, and the values were compared with those in 15 control subjects. RESULTS: Before stress, left ventricular end-diastolic and end-systolic dimensions were reduced, fractional shortening was increased, and the basal septum was thickened (2.3 +/- 0.5 vs. 1.4 +/- 0.2 cm, p < 0.001, vs. control subjects) in the patients, but posterior wall thickness did not differ from that in control subjects. Left ventricular outflow tract diameter, measured as systolic mitral leaflet septal distance, was significantly reduced (13 +/- 4.5 vs. 18 +/- 2 mm, p < 0.001). Isovolumetric relaxation time was prolonged, and peak left ventricular minor axis lengthening rate was reduced (8.1 +/- 3.5 vs. 10.4 +/- 2.6 cm/s, p < 0.05), suggesting diastolic dysfunction. Transmitral velocities and the E/A ratio did not differ significantly. At peak stress, heart rate increased from 66 +/- 8 to 115 +/- 20 beats/min in the control subjects, but blood pressure did not change. Transmitral A wave velocity increased, but the E/A ratio did not change. Left ventricular outflow tract velocity increased from 0.8 +/- 0.1 to 2.0 +/- 0.2 m/s, and mitral leaflet septal distance decreased from 18 +/- 2 to 14 +/- 3 mm, p < 0.001. In the patients, heart rate rose from 80 +/- 12 to 132 +/- 26 beats/min and systolic blood pressure from 143 +/- 22 to 170 +/- 14 mm Hg (p < 0.001 for each), but left ventricular dimensions did not change. Peak left ventricular outflow tract velocity increased from 1.5 +/- 0.5 m/s (at rest) to 4.2 +/- 1.2 m/s; mitral leaflet septal distance fell from 13 +/- 4.5 to 2.2 +/- 1.9 mm (p < 0.001); and systolic anterior motion of mitral valve appeared in 24 patients (80%) but in none of the control subjects (p < 0.001). Measurements of diastolic function did not change. All patients developed dyspnea at peak stress, but none developed a new wall motion abnormality or mitral regurgitation. CONCLUSIONS: Although our patients fulfilled the criteria for "diastolic heart failure," diastolic dysfunction was not aggravated by pharmacologic stress. Instead, high velocities appeared in the left ventricular outflow tract and were associated with basal septal hypertrophy and systolic anterior motion of the mitral valve. Their appearance correlated closely with the development of symptoms, suggesting a potential causative link.     

Left ventricular diastolic filling alterations in subjects with mitral valve prolapse: a Doppler echocardiographic study

To assess left ventricular diastolic filling in mitral valve prolapse (MVP), we studied 22 patients with idiopathic MVP and 22 healthy controls matched for sex, age, body surface area and heart rate. A two-dimensional, M-mode and Doppler echocardiographic examination was performed to exclude any cardiac abnormalities. The two groups had similar diastolic and systolic left ventricular volumes, left ventricle mass and ejection fraction. Doppler measurements of mitral inflow were: E and A areas (the components of the total flow velocity-time integral in the early passive period of ventricular filling, E; and the late active period of atrial emptying, A), the peak E and A velocities (cm.s-1), acceleration and deceleration half-times (ms) of early diastolic rapid inflow, acceleration time of early diastolic flow (AT), total diastolic filling time (DFT) (ms), and the deceleration of early diastolic flow (cm.s-2). From these measurements were calculate: peak A/E ratio (A/E), E area/A area, the early filling fraction, the atrial filling fraction, AT/DFT ratio. All the Doppler measurements reported are the average of three cardiac cycles selected at end expiration. The mean peak A velocity, A/E velocity ratio, deceleration half time and atrial filling fraction were each significantly higher for subjects presenting a MVP (60 +/- 12 cm.s-1 vs 49 +/- 14, P < 0.008; 98 +/- 13% vs 64 +/- 12%, P < 0.0001; 120 +/- 36 ms vs 92 +/- 11, P < 0.002; 0.45 +/- 0.14 vs 0.36 +/- 0.08, P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Midwall fractional shortening is an independent predictor of left ventricular diastolic dysfunction in asymptomatic patients with systemic hypertension

Conventional measures of left ventricular (LV) systolic performance suggest that diastolic dysfunction precedes the development of systolic dysfunction in hypertension. Midwall fractional shortening is a new measure of systolic function that identifies hypertensive patients who have evidence of target-organ damage, impaired contractile reserve, and increased mortality. We therefore sought to determine whether depressed midwall fiber shortening is associated with abnormal diastolic function. Echocardiograms were obtained in 102 otherwise healthy hypertensive patients without treatment with normal conventional measures of systolic function. Of these, 15 had depressed midwall shortening based on previously described normative relations. Patients with depressed midwall shortening had slightly higher blood pressure. Abnormal diastolic function, defined as late (A) LV inflow velocity greater than early (E) velocity, was observed in 33% of those with normal midwall shortening but in 60% of those with depressed shortening (p <0.05). Patients with A/E >1 had lower absolute midwall fiber shortening (15 +/- 3% vs 18 +/- 3%, p <0.0001) but similar endocardial shortening. Patients with abnormal midwall shortening had higher A/E and longer isovolumic relaxation times (both p <0.05). In multivariate analysis, midwall fractional shortening, age, and heart rate were independent predictors (p <0.01) of A/E in a model including blood pressure, LV mass, and endocardial shortening. We conclude that subnormal midwall shortening predicts LV diastolic abnormalities in this population of hypertensive patients with otherwise normal measures of LV systolic function. Contrary to our previous understanding, depressed LV systolic performance, when identified with this newer method, occurs coincidentally with impaired diastolic function.     

The effect of the ingestion of ethanol on obstruction of the left ventricular outflow tract in hypertrophic cardiomyopathy

BACKGROUND: Ethanol causes vasodilation, which might have an adverse effect, due to increased obstruction of the left ventricular outflow tract, in patients with hypertrophic obstructive cardiomyopathy. We assessed the hemodynamic effects of the ingestion of ethanol, in an amount commonly consumed socially, in patients with hypertrophic cardiomyopathy. METHODS: We performed echocardiography in 36 patients before and several times after the ingestion of either 50 ml of 40 percent ethanol or an isocaloric placebo with the aroma of rum. Each patient received both ethanol and placebo, on different days. The patients, but not the physicians, were blinded to the content of the drink. We measured the sizes of the left atrium and left ventricle, the left-ventricular-wall thickness, blood pressure, heart rate, the degree of systolic anterior motion of the mitral valve, and the pressure gradient across the left ventricular outflow tract. RESULTS: The ingestion of ethanol regulated in a significant drop in the mean (+/- SD) systolic blood pressure (from 130.5 +/- 18.6 to 122.5 +/- 20.3 mm Hg, P<0.001), a significant increase in systolic anterior motion of the mitral valve (from a grade of 2.1 to a grade of 2.5, P<0.001), and a 63 percent increase in the mean gradient across the left ventricular outflow tract (from 38.1 +/- 26.5 to 62.2 +/- 42.4 mm Hg, P<0.001). These changes, which were not associated with symptoms, did not occur after the ingestion of placebo. CONCLUSION: The ingestion of a small amount of ethanol caused an increase in the gradient across the left ventricular outflow tract in patients with hypertrophic obstructive cardiomyopathy, which could have and adverse clinical effect.     

Accidental intake of tritiated water: a cytogenetic follow-up case on translocation stability and dose reconstruction

OBJECTIVE: To evaluate the renin-aldosterone system and insulin secretion in hyperparathyroidism and their effects on blood pressure regulation. DESIGN: Studies were carried out on patients with primary hyperparathyroidism (PHPT) prior to and following removal of the parathyroid tumor. METHODS: Sixteen normotensive and euglycemic patients with PHPT were studied. The following parameters were measured: basal and stimulated plasma renin activity (PRA) and aldosterone (ALD) secretion: parathormone (PTH) and serum electrolytes. Insulin and glucose levels were measured during an oral glucose tolerance test. RESULTS: Systolic but not diastolic blood pressure showed a decrease following surgery, from 123.3+/-13.0/80+/-8.6 to 116.7+/-13.5/77.3+/-8.8 mmHg. The decrease in the systolic pressure was not clinically significant. After surgery, both the basal and stimulated PRA and ALD values decreased, and the preoperative pathological values returned to normal: PRA basal: 1.79 --> 0.70 ng/ml/h, P=0.0049; PRA stimulated: 7.76 --> 1.90 ng/ml/h, P=0.0031; ALD basal: 111.5 --> 73.0 pg/ml, P=0.0258; ALD stimulated: 392.5 --> 236.0 pg/ml, P=0.0157. The postoperative decrease in the PRA correlated with the changes in PTH levels (r=0.5442, P < 0.05, n=16) but did not correlate with the changes in serum calcium concentrations. Both the fasting and stimulated insulin levels decreased after surgery but remained within the normal range: insulin fasting: 10.2 --> 5.0 mIU/l, P=0.0218; insulin area under the curve: 5555 --> 3296 mIU/l*min, P=0.0218. There was no correlation between the changes in insulin levels and PTH or ion levels. Sodium, potassium and blood glucose levels remained unaffected by parathyroid surgery. CONCLUSIONS: In a population of normotensive hyperparathyroid patients an increased activity of the renin-aldosterone system related to PTH was found and surgery resulted in a small and insignificant decrease in blood pressure. This change was accompanied by a significant decrease in the activity of the renin-aldosterone system indicating the role of the renin-aldosterone system in the regulation of blood pressure in PHPT. Both fasting and stimulated insulin values decreased following removal of the parathyroid tumor, but with no individual correlation with PTH and calcium levels.     

Excision of a parathyroid adenoma of the aorto-pulmonary window under thoracoscopy

OBJECTIVES: Neck exploration is usually required in all cases of primary hyperparathyroidism. Without a precise localization preoperatively cervicotomy may be unsuccessful, especially in case of an ectopic adenoma. CASE REPORT: A patient with primary hyperparathyroidism due to a solitary adenoma localized in the middle mediastinum was identified on preoperative computed tomography and technetium-99m-sestamibi radionuclide scan. The tumor was successfully removed at thoracoscopy without neck exploration. DISCUSSION: Preoperative localization of primary hyperparathyroid tumors is not indicated in all patients. In some selected cases (acute hypercalcemia, reoperation, serious illness) prior neck exploration would be useful in guiding the surgeon.     

Doppler echocardiographic evaluation of mitral flow velocity and prognosis of cardiac insufficiency

The aim of this study was to determine the role of Doppler echocardiography in establishing the prognosis of Stages to 4 cardiac failure. The echocardiographic indices of left ventricular filling were correlated with catheter data and the 2 year out come of patients. The study population included 54 patients examined prospectively in the context of an evaluation of their cardiac failure. Two years after the initial examination, 19 patients were dead or transplanted. Of the remaining 35 patients, 18 were reevaluated at 6 months. Of the echocardiographic parameters, "hyper normal" mitral flow with a high E/A ration indicated poor prognosis; when E/A > 2, the one year survival was 50% and the 2 year survival 42%. There was overlap between the groups of dead or transplanted and surviving patients only when the E/A ratio was between 2 and 3. The patients with E/A < 2 were all alive without any major events at 2 years. All patients with E/A > 3 had a poor prognosis. The E/A ratio was closely correlated with pulmonary capillary pressure levels (p < 0.001, r = 0.55) and lees closely with cardiac index (p < 0.05, r = 0.4) and radionuclide ejection fraction (p < 0.05, r = 0.28). After 6 months' vasodilator treatment with an angiotensin converting enzyme inhibitor (captopril) the E/A ratio decreased significantly from 1.85 +/- 0.78 to 1.0 0.55 (p < 0.02). A "hyper-normal" mitral flow is related to many factors, including high left ventricular filling pressures, mitral regurgitation and reduced left ventricular compliance. This appearance of mitral flow is a poor prognosis factor in severe cardiac failure.     

Significance of radiographic cardiomegaly in orthotopic heart transplant recipients

OBJECTIVE: The purpose of this study is to evaluate the clinical significance of radiographic cardiomegaly in orthotopic heart transplant recipients and to identify causative anatomic and physiologic parameters. MATERIALS AND METHODS: We retrospectively compared the cardiothoracic ratio (CTR) measured using standard posteroanterior chest radiography with left ventricular end-diastolic diameter and left ventricular ejection fraction measured on two-dimensional echocardiography; right ventricular systolic pressure; and systolic, diastolic, and mean blood pressure measured at biopsy in 46 heart transplant recipients. RESULTS: Twenty-eight (61%) of the 46 patients had radiographic cardiomegaly. When we compared heart transplant recipients who had a CTR greater than 0.5 with recipients who had a CTR less than or equal to 0.5, we found no significant difference between their respective left ventricular end-diastolic diameters, left ventricular ejection fractions, right ventricular systolic pressures, systolic blood pressures, or mean blood pressures. A statistically significant difference existed between the mean values of diastolic blood pressure for transplant recipients with and without radiographic cardiomegaly. We found no significant correlation between CTR and left ventricular end-diastolic diameter, left ventricular ejection fraction, systolic blood pressure, diastolic blood pressure, or mean blood pressure. CONCLUSION: The statistically significant difference between the mean values of diastolic blood pressure of transplant recipients with and without radiographic cardiomegaly is clinically insignificant and unlikely to account for the finding of radiographic cardiomegaly. We conclude that radiographic cardiomegaly, which occurs frequently in heart transplant recipients, does not correlate with anatomic or physiologic parameters obtained under the same conditions. Radiographic cardiomegaly in heart transplant recipients does not connote allograft dysfunction or heart failure.     

Isotypic antibody responses of a population in an endemic area of schistosomiasis japonica and their epidemiologic significance

OBJECTIVE: Chordal transposition was advocated for correction of anterior mitral prolapse. We have evaluated the early and late results of this technique in different anatomical presentations. METHODS: From 1986 to 1995, 185 mitral valve repairs were carried out for pure mitral regurgitation due to a degenerative disease. Eighty-nine patients had either an anterior prolapse (39) or prolapse of both leaflets (50) at initial presentation and underwent chordal transposition from the mural leaflet to the anterior leaflet. The corrective procedure was completed by polytetrafluoroethylene or pericardial posterior annuloplasty. Twenty patients presented a complex pathology and 26 had chordal elongation of mural leaflet. Annular calcifications were found in 9 patients. Seven patients required shortening of transposed chordae and two patients the additional shortening of an anterior chorda. RESULTS: Operative mortality was 3.3% and follow-up was 95% complete (average 41 months). There were five postreconstruction valve replacements (two earlier and three later) for a probability of freedom from late reoperation or 3+ mitral regurgitation of 88.6 +/- 4.8% at 5 years. Of the patients 79% presented no or trivial residual MR, 17% moderate MR and 4% severe MR. The presence of a complex pathology or posterior chordal elongation did not influence the entity of postoperative residual regurgitation. On the contrary, the patients with annular calcifications had a residual regurgitation/left atrium area ratio greater than patients without annular calcification (15.8 +/- 11.5% vs. 6.1 + 9.9%; P = 0.009). CONCLUSIONS: Chordal transposition is an effective and easily carried out technique for the correction of anterior mitral prolapse. The presence of a complex pathology or posterior chordal elongation do not rule out the procedure. The absence of annular calcification is important in order to obtain a satisfactory correction.     

Estimation of left ventricular end-diastolic pressure with the difference in pulmonary venous and mitral A durations is limited when mitral E and A waves are overlapped

Previous studies showed that difference in pulmonary venous and mitral A-wave durations can be used for the estimation of left ventricular end-diastolic pressure, which is based on the assumption that the pulmonary venous A wave and mitral A wave start with the beginning of left atrial contraction. It is also assumed that the mitral A wave ends with the end of left atrial contraction. These assumptions may not be correct if left atrial contraction occurs before the early left ventricular filling is completed. Adequate Doppler mitral inflow and pulmonary venous flow signals were obtained simultaneously with left ventricular pressures at the cardiac catheterization laboratory in 50 patients who showed separated E and A waves in mitral inflow. After heart rate was increased by right atrial pacing to make the mitral E and A waves overlap, Doppler and hemodynamic measurements were repeated. When E and A waves are separated, pulmonary A-wave duration exceeding mitral A-wave duration has a sensitivity of 67% and specificity of 85% in the prediction of elevated left ventricular end-diastolic pressure (>/=20 mm Hg), whereas the pulmonary A wave ending later than mitral A wave has a sensitivity of 83% and a specificity of 45%. When the mitral E and A waves are overlapped, the pulmonary A wave ending later than mitral A wave is better for the prediction of elevated left ventricular end-diastolic pressure (sensitivity 55%, specificity 75%) than pulmonary A-wave duration exceeding mitral A-wave duration (sensitivity 9%, specificity 96%). However, overall, both methods are limited for clinical use.     

Two-year follow-up study to evaluate the reduction of left ventricular mass and diastolic function in mild to moderate diastolic hypertensive patients

OBJECTIVE: To compare the effects of two antihypertensive agents, amlodipine and lisinopril, on left ventricular mass and diastolic filling in patients from primary care centers with mild to moderate diastolic hypertension. STUDY DESIGN: A second-year, open follow-up of a prospective, double-blind, randomized, parallel group, comparative study. METHODS: Male and female patients between 25 and 75 years-of-age with elevated diastolic blood pressure (four measurements > or = 95 mmHg from multiple measurements taken on three occasions and average diastolic blood pressure < 115 mmHg) were recruited from a population survey. After 4 weeks' placebo run-in, 71 patients were included of whom 60 finished the first study year and 51 finished the second study year. Patients were randomly assigned to receive doses of 5-10 mg amlodipine or 10-20 mg lisinopril, which were titrated on the basis of the effects on blood pressure. Primary endpoints were left ventricular mass index (LVMI) and early to atrial peak filling velocity. Office and ambulatory blood pressure were considered secondary endpoints. RESULTS: The decrease in blood pressure was equal for both treatment regimens in the first year. A statistically significant (P< 0.001) decrease in LVMI in both treatment groups was observed in the first year [-11.0 g/m2 (95% Cl -6.0 to -16.1) in the amlodipine group and -12.6 g/m2 (95% Cl -8.2 to -17.0) in the lisinopril group]. Early to atrial peak filling velocity did not change significantly within the treatment groups in the first year [+0.07 (95% CI -0.01 to +0.15) in the amlodipine group and +0.01 (95%9 Cl -0.06 to +0.08) in the lisinopril group. Blood pressure, LVMI and early to atrial peak filling velocity did not change in the second year of treatment. No significant differences in primary and secondary endpoints between treatment groups were found in the first or second year. Conclusion: The effects of amlodipine and lisinopril on left ventricular mass and early to atrial filling peak velocity after 2 years of treatment were similar and these effects were already observed after 1 year of treatment. Additional studies of longer duration (> or = 4 years) and with a larger sample size are recommended.     

Atherosclerosis and left ventricular hypertrophy: persisting problems in treated hypertensive patients

OBJECTIVES: First, to determine whether hypertensive patients managed in general practice have more advanced atherosclerosis and left ventricular hypertrophy than matched normotensive patients from the same practices. Second, to investigate the associations of several potentially modifiable factors with these vascular and cardiac outcomes. DESIGN AND METHODS: We performed a case-control study of 500 hypertensive cases (systolic blood pressure > or = 160 mmHg or diastolic blood pressure > or = 95 mmHg or receiving treatment) and 506 age- (mean 61 years) and sex- (54% female) matched normotensive controls recruited from general practices. Carotid artery far wall thickness (CWT), assessed by B-mode ultrasound, and left ventricular mass (LVM), assessed by M-mode echocardiography, were the main study outcome measures. RESULTS: Mean systolic/diastolic blood pressure levels in the 399 treated cases (145/87 mmHg) were lower than those in untreated cases (158/94 mmHg) but higher than those in controls (133/82 mmHg, all P < 0.0001). Mean body mass index (BMI) and total triglyceride levels were higher and high-density lipoprotein cholesterol was lower in cases than in controls (all P < 0.0004). Mean CWT was 10% greater in cases than in controls and LVM was 14% greater (both P < 0.001), but both were similar in treated and untreated cases (P > 0.05). In multivariate analyses, blood pressure and BMI were both directly and independently related to CWT and LVM (both P < 0.0001). CONCLUSIONS: In this study, hypertensive patients managed in general practice - whether treated with antihypertensive drugs or not - had more advanced atherosclerosis and left ventricular hypertrophy than did matched normotensive patients. Efforts to lower blood pressure further and to reduce BMI could potentially reduce these differences, and this might lead to a reduction in the risk of major cardiovascular events.     

Angiotensin-converting enzyme (ACE) inhibitors revert abnormal right ventricular filling in patients with restrictive left ventricular disease

OBJECTIVES: Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure. BACKGROUND: It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I). METHODS: Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. RESULTS: Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45+/-6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30+/-5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01). CONCLUSIONS: Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.     

Hypercalcemic cardiomyopathy associated with primary hyperparathyroidism mimicking primary obstructive hypertrophic cardiomyopathy

A 72-year-old woman presented to hospital with rapidly progressive dyspnea and chest pain on exertion. Physical findings included a grade 3/6 systolic murmur increased by the Valsalva manoeuvre. Transthoracic echocardiography revealed concentric left ventricular hypertrophy, systolic anterior motion of the mitral valve and critical dynamic outflow tract obstruction. The myocardium was strikingly heterogeneous with hyperdynamic left ventricular systolic function. Laboratory findings included severe hypercalcemia secondary to primary hyperparathyroidism. The patient's outcome was unfavourable with nephrogenic diabetes insipidus, pancreatitis, shock, severe acidosis and death. Postmortem examination confirmed the presence of severe concentric left ventricular hypertrophy, a narrowed left ventricular outflow tract and localized endocardial fibrosis of the left interventricular septum. Microscopic findings showed diffuse calcium deposits of the myocardium, coronary arteries, kidneys and lungs. This appears to be the first report of two-dimensional and Doppler echocardiographic findings in hypercalcemic cardiomyopathy mimicking obstructive hypertrophic cardiomyopathy.     

Unidirectional valve patch for repair of cardiac septal defects with pulmonary hypertension

BACKGROUND: Congenital septal defects with a large left-to-right shunt often cause pulmonary hypertension, which complicates surgical repair of the defects. METHODS: Twenty-four patients with congenital cardiac septal defects and severe pulmonary hypertension had operation to close the septal defect using a unidirectional valve patch during a 3-year period. The ratio of systolic pulmonary artery pressure to systolic arterial blood pressure was near to or more than 1.0 in all patients. RESULTS: Two patients died in the hospital after operation, and there have been no deaths during intermediate term follow-up. Mean pulmonary artery pressure decreased from 80 +/- 12 mm Hg to 56 +/- 18 mm Hg. The ratio of pulmonary artery pressure to systemic arterial pressure dropped from 1.1 +/- 0.1 mm Hg to 0.7 +/- 0.1 mm Hg. The unidirectional valve patch functioned allowing right to left shunting in 4 patients with a systolic pulmonary artery pressure more than systolic arterial blood pressure immediately after closure of a septal defect. The patch sealed or was effectively closed by the third postoperative day. There was impressive improvement in symptoms and exercise tolerance after operation during the 3-month to 3-year (mean, 1.1 year) follow-up period. CONCLUSIONS: The unidirectional valve patch is useful for management of patients having operation to close cardiac septal defects in the presence of severe pulmonary hypertension.     

Effects of obesity and weight loss on cardiac function and valvular performance

OBJECTIVE: To study the consequences of long-standing obesity on myocardial function and valvular performance and to determine the effects of weight loss on these cardiovascular features. RESEARCH METHODS AND PROCEDURES: We included 41 patients with obesity referred for weight-reducing gastroplasty, 31 patients with obesity who received dietary recommendations, and 43 lean subjects. Body weight and blood pressure were measured, and cardiac function and valvular performance were estimated echocardiographically. Left ventricular ejection fraction was used to assess systolic heart function, and the ratio of transmitral early to atrial (E/A) peak flow velocity was used as an estimate of diastolic filling. All three study groups were investigated at baseline, and the two groups with obesity were re-examined at 1-year follow-up. RESULTS: Patients with obesity had higher blood pressure, greater cardiac output, lower ejection fraction, and reduced E/A ratio, compared with lean subjects (p<0.01). Surgical treatment of obesity led to significant decreases in body weight, whereas body weight remained unchanged in the group treated with dietary recommendations (p<0.001). In the weight loss group, blood pressure and cardiac output decreased and the E/A ratio increased (p<0.001). Left ventricular ejection fraction tended to increase in the weight loss group and decrease in the obese control group (p<0.01). No significant valvular disease was observed in any of the subjects with obesity at baseline or after weight loss. DISCUSSION: We conclude that weight reduction in subjects with obesity is associated with improvements in left ventricular diastolic filling and has favorable effects on left ventricular ejection fraction. Neither obesity nor weight loss seem to promote valvular heart disease.