Impact of ß-thalassemia trait carrier state on cardiovascular risk factors and metabolic profile in patients with newly diagnosed hypertension.

Thalassemia minor (Tm), the ß-thalassemia carrier state, is followed by favorable lipidemic profile and seems to protect against myocardial infarction mainly in men. However, the cardiovascular risk factor (CRF) and metabolic profile of these subjects has not been thoroughly addressed, although it is not known whether gender differences are involved. We evaluated CRFs, metabolic parameters and risk-prediction equations along with renal function and selected echocardiographic indices in 23,680 consecutive subjects, that is, 11,192 women and 12,488 men, with newly diagnosed hypertension according to the presence or absence of Tm. Of 23,680 patients, 548 (2.3%) had Tm. Compared with patients without Tm, Tm cases had similar gender distribution, age, body mass index and blood pressure. Besides having a better lipidemic profile, Tm patients were less frequently smokers (25% vs. 32%, P<0.001), had a lower prevalence of metabolic syndrome (26% vs. 39%, P<0.001) and lower HeartSCORE and INTERHEART scores (P<0.001). Tm patients also had lower levels of fibrinogen and plasminogen activator inhibitor-1 (P<0.001), lower serum creatinine and higher estimated glomerular filtration rate (P<0.001), lower prevalence of left ventricular hypertrophy (35% vs. 48%, P<0.001) and higher total and mid-wall fractional shortening (P=0.03 and <0.001, respectively). Most of these differences were consistent in both genders, whereas the HeartSCORE and the echo indices were significantly better in Tm only in women. Among patients with newly diagnosed hypertension, those with Tm have a better overall CRF and metabolic profile, beyond the well-known differences in serum lipids. Compared with men, women seem to be at least equally protected.

Cardiovascular risk factor(s) prevalence in Greek hypertensives. Effect of gender and age.

The aim of this study was to determine cardiovascular (CV) risk factors (RFs) and target organ damage clustering in 21280 Greek hypertensives stratified by gender and age. Glycemic and lipid profile were determined, left ventricular mass index, estimated gromerular filtration rate (eGFR), 10-years CV risk according to Framingham risk score (FRS) and HeartScore (HS) were calculated. Only 10.2% of patients had no concomitant RFs, 53.1% had one (48.8% dyslipidemia, 3.4% smoking, 0.9% diabetes), 32.9% had two (26% dyslipidemia and smoking, 6.6% dyslipidemia and diabetes, 0.3% smoking and diabetes) and 3.7% had all four traditional RFs. Obesity was present in 30%, metabolic syndrome in 38%, low eGFR in 24% and left ventricular hypertrophy in 49%. Mean FRS risk was 35% for males, 24.1% for females whereas in high risk (>20%) were 68.7 and 50.7%, respectively (P<0.0001). Mean HS risk was 8.4% for males, 6.2% for females whereas in high risk (>5%) were 48.6 and 36.2%, respectively (P<0.0001). Age was correlated to pulse pressure, eGFR, left ventricular mass index and CV risk (P<0.0001). Ageing increased the risk difference between genders for total (P=0.001) but not for fatal events (P=nonsignificant). In conclusion, as RFs cluster in hypertensives, CV risk calculation should guide treatment decisions.

Differential pulse pressure response to various antihypertensive drug families.

Pulse pressure (PP) is emerging as a major pressure predictor of cardiac disease. The study comprised 10 185 untreated patients with essential hypertension. A total of 5395 men and 4790 women 56+/-13 years old, with uncomplicated essential hypertension, after a 15-day washout period and after 6 months of antihypertensive monotherapy were included. All patients included in the final cohort were responders and had normalized their blood pressure. PP was decreased least with diuretics (-5 mm Hg) and most with angiotensin II receptor blockers (ARBs) and calcium antagonists (-15 mm Hg), followed by angiotensin-converting enzyme inhibitors (ACEI) (-12 mm Hg) alpha- and beta-blockers (-10 and -9 mm Hg), differentiating among antihypertensive classes (P<0.001). The magnitude of PP fall was related to the degree of left ventricular (LV) mass reduction (P<0.001), seen best with ARBs (r=0.42) and least with ACEIs (r=0.18). Of the antihypertensive medications used in everyday practice, PP decrease may be achieved best with ARBs and calcium antagonists, whereas diuretics confer poor response. PP was decreased least with diuretics (-5 mm Hg) and most with ARBs and calcium channel blockers (-15 mm Hg), followed by ACEI (-12 mm Hg) alpha- and beta-blockers (-10 and -9 mm Hg), differentiating among antihypertensive classes (P<0.001). Of the antihypertensive medications used in everyday practice, PP decrease may be achieved best with ARBs and calcium antagonists.

Mild left ventricular hypertrophy in essential hypertension: is it really arrhythmogenic?

Left ventricular hypertrophy (LVH) has been associated with an increased incidence of ventricular arrhythmias and sudden cardiac death in hypertensive patients. However, it is not known whether this relationship exists in early asymptomatic hypertensives with mild LVH. We prospectively examined 100 consecutive patients with essential hypertension, 35 without and 65 with mild LVH on echocardiography. All underwent a detailed noninvasive arrhythmia work-up and were subsequently followed-up for 3 +/- 1 years in an ambulatory hypertension clinic. None of the 12-lead electrocardiographic parameters examined differed between the two hypertensive groups. A similarly low incidence of simple forms of ventricular ectopy was present in both groups, whereas complex forms of ventricular ectopy were extremely rare in either group. The signal-averaged electrocardiographic parameters examined were also not significantly affected by the presence of mild LVH. Arrhythmia-related symptoms or malignant ventricular arrhythmia events were not observed in either group of patients during follow-up with antihypertensive treatment. The latter resulted in LVH regression in the 65 patients with mild LVH at baseline. It appears that mild LVH among ambulatory hypertensive patients does not carry an additive arrhythmogenic risk and can be successfully reversed with the appropriate antihypertensive therapy, with no need of additional antiarrhythmic management.

Regression of left ventricular hypertrophy results in improvement of QT dispersion in patients with hypertension.

OBJECTIVES: Increased QT dispersion has been considered as predisposing to ventricular arrhythmias in hypertrophic cardiomyopathy, congestive heart failure, and coronary artery disease. An increased QT dispersion has also been found in hypertensive patients with left ventricular hypertrophy (LVH). The data on the effect of LVH regression on QT dispersion are limited. METHODS AND RESULTS: To assess the relation of LVH regression and QT dispersion decrease, 68 patients (42 men and 26 women, mean age 56.3+/-9.5 years) with uncomplicated essential hypertension were studied. All underwent full electrocardiographic and echocardiographic studies at baseline and after 6 months of monotherapy, 29 with angiotensin-converting enzyme inhibitors and 39 with calcium antagonists. QT dispersion was calculated by subtracting the shortest QT from the longest QT, in absolute value (QTmax - QTmin). It was also corrected with Bazett's formula (QTc dispersion). Left ventricular mass index was assessed according to the Devereux formula. After treatment, LVH decreased with both angiotensin-converting enzyme inhibitors (from 155 to 130 g/m2, P < .001) and calcium antagonists (156 to 133/92/m2, P < .001). QT dispersion decreased both after angiotensin-converting enzyme inhibitor treatment (from 82 to 63 ms) and calcium antagonist treatment (from 77 to 63 ms, both P < .001 ). There was a significant correlation of QT dispersion and left ventricular mass after therapy (r = 0.36, P < .005). There was a correlation of the degree of LVH and QT dispersion decrease (r = 0.27, P < .05). CONCLUSIONS: It is concluded that LVH regression influences AQT favorably. Its prognostic value has yet to be determined.

Significance of blood pressure levels achieved with felodipine anti-hypertensive treatment on cardiovascular structure and function changes.

One of the targets of anti-hypertensive treatment is cardiovascular structural and functional improvements, while the level of blood pressure (BP) under treatment is related to patient morbidity and mortality. The aim of this study was to evaluate the relation of BP achieved after felodipine monotherapy to the degree of cardiovascular changes. Six hundred patients with essential hypertension were studied and grouped according to diastolic BP (DBP) levels after 6 months of therapy: 90-94 (n = 86), 85-89 (n = 186), 80-84 (n = 180) and < 80 mm Hg (n = 148). Overall BP fell from 175/103 to 137/83 mm Hg with a concomitant moderate reflex tachycardia (3.3%). Left ventricular (LV) dimensions decreased to a degree (-0.4 and -0.8%, P < 0.0001), with the greatest decrease in patients with lower DBP levels under treatment (P < 0.0001). LV systolic function improved to a modest degree (0.8%, P < 0.0001), depending on DBP fall (P < 0.0001), as did cardiac output (2.4%, P < 0.0001). LV systolic wall stress and total peripheral resistance fell (-18% and -14%, P < 0.0001) in relation to DBP drop (P < 0.0001), as did aortic root distensibility (55%, P < 0.0001). It is concluded that the degree of cardiovascular structure and function improvements are directly related to the DBP levels achieved under felodipine anti-hypertensive therapy.

Exercise-induced ST-segment variability may discriminate false positive tests.

The clinical value of exercise-induced variations in ST-segment depression and R wave amplitude in consecutive sinus beats was studied in 160 patients who had a positive treadmill exercise test with the Bruce protocol. The patients, all of whom underwent cardiac catheterization, included 100 with coronary artery disease (CAD) (group with true positive test) and 60 with normal coronary arteries (group with false positive test). Minimal or no exercise-induced variations in the magnitude of ST-segment depression despite variations in R wave amplitude were observed in 84 of the 100 patients with CAD and in only 9 of the 60 patients with normal coronary arteries (P < .0001). Significant exercise-induced variations in ST-segment depression were observed in only 16 of 100 patients with CAD and in 51 of 60 patients with normal coronary arteries (P < .0001). The coefficient of variation of R wave amplitude was similar in both groups (no statistical significance), while the coefficient of variation of ST-segment depression was much greater in the patients with normal coronary arteries than in those with CAD (P < .0001). It is concluded that variability of ST-segment depression at peak exercise may discriminate false positive from the true positive exercise tests, improving the diagnostic ability of the method.

Acute changes of left atrial distensibility in congestive heart failure.

BACKGROUND: Investigations of the left atrial (LA) distensibility have revealed that it plays a major role in atrial function; however, LA distensibility has not as yet been studied in congestive heart failure (CHF). HYPOTHESIS: The study was undertaken to determine the effects of acute administration of esmolol, isosorbide dinitrate, dobutamine, and normal saline infusion on LA dimension, pressure, and distensibility. METHODS: The study included 23 patients with CHF (18 with ischemic heart disease and 5 with idiopathic dilated cardiomyopathy). Left atrial diameters (D) and pressures (P) were recorded at rest and thereafter during acute tests. P and D data during the ascending limb of the V loop were fitted to the exponential function P = b.ead, where a is the passive elastic chamber stiffness constant and b is the elastic constant. The instantaneous diastolic LA distensibility (IDLAD) was calculated as 1/(dP/dD) = 1/a.P. RESULTS: The constant, a, increased significantly after normal saline and esmolol infusion (p < 0.001), while it significantly decreased after isosorbide dinitrate (p < 0.001) and dobutamine administration (p < 0.05) compared with baseline. Instantaneous diastolic LA distensibility (in mm/Hg) was 0.16 at baseline; it significantly increased after isosorbide dinitrate (0.32) and dobutamine (0.24) administration, while it significantly decreased after normal saline (0.11) and esmolol (0.12) infusion (p < 0.001 for all). CONCLUSION: In CHF, LA distensibility may acutely increase with vasodilators or inotropics or may decrease with beta blockade or volume loading.

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.

Arterial blood pressure changes in children and adolescents with insulin-dependent diabetes mellitus.

Diabetic nephropathy may develop in childhood and is often related to hypertension. The 24-hour ambulatory blood pressures were measured in 63 children with insulin-dependent diabetes mellitus and were compared with those of 54 healthy siblings. The patients were without clinical complications. The 24-hour recording of their blood pressures revealed higher 24-hour systolic blood pressure (SBP) (115.8 +/- 8.2), 24-hour diastolic blood pressure (DBP) (67.5 +/- 4.6), 24-hour mean arterial pressure (MAP) (81.8 +/- 5.2) compared with control subjects: 24-hour SBP (112.7 +/- 6.7), 24-hour DBP (64.7 +/- 4.1), 24-hour MAP (78.9 +/- 4.5) (p = 0.03, p = 0.001, p = 0.002, respectively). Of the daytime blood pressures, SBP, DBP, MAP were also higher (117.7 +/- 8.7, 69.7 +/- 5.2, 83.8 +/- 5.8) compared with those of siblings (114.9 +/- 6.9, 67.3 +/- 4.3, 81.1 +/- 4.9) (p = 0.05, p = 0.009, p = 0.008, respectively). Of the nighttime blood pressures, SBP, DBP, MAP were higher in patients (108.7 +/- 8.9, 59.5 +/- 6.9, 74.6 +/- 6.9) compared with control subjects (104.8 +/- 7.0, 55.1 +/- 5.0, 70.5 +/- 5.1) (p = 0.01, p = 0.0002, p = 0.0006, respectively). Furthermore, the blood pressure burden was evaluated. Blood pressure burden was defined as the percentage of the increased blood pressure readings greater than the 95th percentile divided by the total number of recorded blood pressures during a corresponding period. Patients had a 43% higher 24-hour SBP burden (19.6 +/- 16.5) and a 50% higher 24-hour DBP burden (12.3 +/- 9.6) in relation to that of control subjects (13.7 +/- 12.8, 8.3 +/- 12.3) (p = 0.03, p = 0.009, respectively). The SBP burden (17.9 +/- 14.6) and DBP burden (11.5 +/- 9.2) of the day was approximately 50% higher in the patients in the relation to control subjects (11.9 +/- 11.1, 7.8 +/- 6.7) (p = 0.01, p = 0.01, respectively). Therefore it seems that hemodynamic changes may appear early in children with diabetes.

Effects of menopause on aortic root function in hypertensive women.

OBJECTIVES: This study sought to determine whether the natural decrease in sex hormones that occurs during menopause in hypertensive women plays a role in aortic root stiffness. BACKGROUND: The effect of menopause-induced sex hormone deprivation on aortic root function is not known; however, it is of special interest in hypertensive subjects, whose aortic elastic properties are already compromized. METHODS: Eighteen women with essential hypertension were followed-up for 3 years, during which time they went through menopause (group A) and were compared with 22 age-matched hypertensive women with normal menses (group B) and 20 hypertensive men (group C). Blind echocardiographic tracings and simultaneous blood pressure measurements were obtained after at least 30 medication-free days, both at baseline and 3.5 years later. RESULTS: Aortic root function tended to be aggravated in both groups B and C, but not significantly so, with no between-group differences (p = NS), whereas it deteriorated in group A. Thus, in menopausal hypertensive subjects, aortic root systolodiastolic percent change decreased (from 6.7% to 4.9%, p < 0.0001 [p = 0.002 vs. group B; p = 0.006 vs. group C]); cross-sectional compliance decreased (from 18 to 13 cm2/mm Hg, p < 0.0001 [p = 0.002 vs. group B; p = 0.03 vs. group C]); Peterson's elastic modulus increased (from 1.2 to 1.9 dynes/cm2, p = 0.0006 [p = 0.003 vs. group B; p = 0.005 vs. group C]); aortic stiffiness index increased (from 7.0 to 10.8, p = 0.0008 [p = 0.004 vs. group B; p = 0.007 vs. group C]); and aortic root distensibility decreased (from 1.8 to 1.2 dynes/cm2, p < 0.0001 [p = 0.0003 vs. group B; p = 0.007 vs. group C]). Serum lipids did not change significantly in any group (p = NS). CONCLUSIONS: In hypertensive women, the effect of menopause on the elastic properties of the aortic root is abrupt and devastating.

Myocardial trophic effects of blood pressure in children with insulin-dependent diabetes mellitus.

To evaluate the effect of blood pressure (BP) on the left ventricular mass index (LVMI), 66 children with IDDM 13 +/- 3 years of age were studied and compared with 58 healthy age-matched siblings. The 24 h BP recordings disclosed that children with diabetes had higher DBP (68 vs. 65 mm Hg, P = 0.002), especially at night (60 vs. 55 mm Hg, P = 0.00007), with a minimisation of the normal nocturnal hypotension (-9.9 vs. -12.4 mm Hg, P = 0.04). Their LVMI was higher (79 vs. 71 g/m2, P = 0.02); it was independent of BP values and variability (P = NS), but it was positively correlated with heart rate (r = -0.46, P = 0.0005). In the control group, LVMI was significantly correlated with the mean SBP (r = 0.46, P = 0.0005); with its variability (r = 0.32, P = 0.02) and, to a lower extent, with heart rate (r = -0.29, P = 0.03). It is concluded that in children with diabetes mellitus the participation of BP in myocardial hypertrophy is not so obvious, although the BP load is increased. The increase of the LVMI occurs early in life and before the onset of hypertension.

Left ventricular and aortic root structure and function changes with beta blocker antihypertensive therapy. A one-year double blind study of celiprolol and metoprolol.

Using echocardiographic and Doppler methodology, we evaluated the effects of celiprolol 200-400 mg/day and metoprolol 100-200 mg/day, given for one year, on haemodynamics, left ventricular structure and function, and aortic root distensibility in 40 hypertensive patients. Total peripheral resistance was unchanged with metoprolol (-1.7%) but decreased with celiprolol (-11.2%), a significant difference between the two treatments (P = 0.01). Left ventricular mass index was reduced by 5.7% in those patients receiving metoprolol and by 11.8% in those receiving celiprolol (P < 0.001). Cardiac index fell significantly with metoprolol and marginally with celiprolol (-13.9% vs. 5.9%, P = 0.003). Left ventricular diastolic function-as shown by the transmitral early to late peak filling velocity ratio-was not altered with metoprolol, but a significant increase (17%, P = 0.2) was seen with celiprolol. Both metoprolol and celiprolol increased aortic root distensibility, with celiprolol having a significantly greater effect (80% vs. 30%, P < 0.01). We conclude that, in comparison to metoprolol, long term antihypertensive therapy with celiprolol improves left ventricular diastolic and aortic root function, whilst reducing total peripheral resistance and left ventricular hypertrophy.

Effect of beta-blockade on exercise capacity in hypertensive subjects: a one-year double-blind study of celiprolol and metoprolol.

To assess the effect of beta-blocker antihypertensive therapy on exercise capacity, 40 patients randomized to celiprolol 200 mg and metoprolol 100 mg daily in a double-blind fashion were studied after a month of placebo and a year of active treatment. Both drugs normalized office blood pressure and produced echocardiographic and electrocardiographic left ventricular hypertrophy regression. In symptom-limited maximal stress tests before and after treatment, exercise duration increased with (p < 0.0001) celiprolol (513-700 seconds) and metoprolol (520-634 seconds), although more with the former (p = 0.02). Resting heart rate was reduced with both, more with metoprolol (p < 0.001), while heart rate at peak exercise was reduced similarly with both medications (p < 0.005). Blood pressure at peak exercise was reduced with both celiprolol (217-184 mmHg; p = 0.0002) and metoprolol (218-185 mmHg, p < 0.0001) to a similar degree (p = NS). Exercise parameters were not related to patient age or the degree of left ventricular hypertrophy regression (p = NS). It is concluded that beta-blocker antihypertensive therapy improves exercise capacity, decreasing heart rate and blood pressure responses to stress, irrespective of left ventricular structural changes.

Ambulatory blood pressure changes in the menstrual cycle of hypertensive women. Significance of plasma renin activity values.

Blood pressure (BP) changes during the menstrual cycle (MC) have not been studied in hypertensive women in relationship to changes in sex hormone levels and plasma renin activity (PRA). We therefore carried out 24 h ambulatory BP recordings and hormonal measurements in 34 hypertensive and 27 matched normotensive women during the follicular ovulatory and luteal phases of the menstrual cycle. Plasma renin activity was similar in the two groups and rose significantly during the luteal phase only in the hypertensives (P < .01). There were no differences in plasma estradiol or progesterone between the normotensives and hypertensives, but testosterone was higher in the hypertensives during the ovulatory (P < .01) and luteal (P < .001) phases. Blood pressure did not change in the normotensives throughout the cycle, but it increased in the hypertensives during ovulation (P < .01). When patients were divided according to mean menstrual cycle PRA, only those with relatively low PRA (< 2 ng/mL/h) had a significant BP rise during ovulation and it primarily occurred at night (P < .05). The results demonstrate that premenopausal hypertensive women have increased testosterone during ovulation and increased testosterone and PRA during the luteal phase of the cycle. Like normotensives, hypertensives with relatively high PRA exhibit no change in BP during the cycle, whereas those with relatively low PRA have a nighttime increase in BP during ovulation.

Significance of R wave changes in exercise-induced supraventricular extrasystoles. Angiographic correlates.

To evaluate the clinical significance of observed R wave amplitude changes in exercise-induced supraventricular extrasystoles in comparison to the preceding sinus beat, 94 patients catheterized for possible coronary artery disease (CAD) were studied. Significant CAD was documented in 63 patients--34 with myocardial infarction (group A1) and 29 without (group A2)--whereas 31 patients had normal coronary arteries or coronary lesions less than 30% (group B). All patients underwent treadmill stress testing using the Bruce protocol within a month after cardiac catheterization. R wave amplitude increased or remain unchanged in extrasystole (R(x-s) > or = 0) in patients with CAD, while it decreased (negative R(x-s) in patients without significant CAD (P < .0001). In patients with CAD R(x-s) values were positively related to the number of obstructed coronary arteries (P < .01), while no significant difference was found between groups A1 and A2. The correlations of R wave amplitude changes in extrasystoles were significant with coronary obstruction score values (r = .82 and .85 in groups A1 and A2, respectively) and with left ventricular ejection fraction values (r = -.88, -.86 and -.90 in groups A1, A2, and B, respectively). R(x-s) > or = 0 value had a sensitivity of 79% and a specificity of 90% for CAD detection, while sensitivity was higher (89%) and specificity was lower (57%) for the prediction of left ventricular dysfunction. It is concluded that R(x-s) > or = 0 value is indicative of CAD, multivessel disease, and poor left ventricular performance, while its negative value is combined with minimal or no CAD and normal ejection fraction values.

Regression of left ventricular hypertrophy with isradipine antihypertensive therapy.

To assess left ventricular (LV) structural and functional changes, 45 hypertensive patients were studied by echocardiography after 2 weeks of placebo and 6 months of isradipine monotherapy. Although LV cavity size did not change, LV wall thickness decreased dramatically (P < .0001), producing a significant decrease in LV mass index (from 158 g/m2 to 136 g/m2; P < .0001). In addition, LV fractional shortening (FS) did not change (1.2%; P = NS) whereas the cardiac index increased (6.4%; P = .0007) due to a modest tachycardia accompanied by a reduction in total peripheral resistance (-22.1%; P < .0001). The magnitude of the reduction of LV mass was related to the degree of FS increase (r = -0.70; P < .0001), an indication of beneficial LV remodeling. It can be concluded that isradipine antihypertensive therapy leads to regression of LV hypertrophy without depression of LV pump function.

Exercise-induced S-wave prolongation in left anterior descending coronary artery stenosis.

Myocardial ischemia may decrease conduction velocity and produce QRS prolongation in the surface electrocardiogram. In cases with normal intraventricular conduction, areas of the myocardium contributing to the development of the S wave receive blood from all 3 major coronary arteries, whereas in left anterior hemiblock or right bundle branch block, most of the blood supply to the areas of the myocardium contributing to the development of the S wave is from the left anterior descending (LAD) coronary artery. To test the hypothesis that the S wave will be prolonged with exercise only in patients with LAD coronary artery stenosis and left anterior hemiblock or right bundle branch block, 88 patients with normal intraventricular conduction, 66 with left anterior hemiblock and 36 with right bundle branch block were studied. Sixty-four, 32 and 21 patients had LAD, right and left circumflex coronary artery stenoses, respectively. In patients with normal coronary arteries, S-wave duration decreased with exercise regardless of the status of ventricular conduction. In patients with coronary artery disease and normal intraventricular conduction, the S wave was prolonged slightly with exercise, but in those with left anterior hemiblock and right bundle branch block, it was prolonged significantly (12.5 +/- 6 and 10.4 ms, respectively) only in those with LAD, but not in those with circumflex or right coronary artery stenosis. S-wave prolongation in patients with LAD coronary artery stenosis and left anterior hemiblock or right bundle branch block most likely is related to exercise-induced ischemia in the areas of the myocardium contributing to the development of the S wave.