Arterial hypertension increases left ventricular mass: role of tight blood pressure control

In middle-age hypertensives from the Gubbio Population Study, we evaluated the relationship between blood pressure (BP) control over a long time and the prevalence of left ventricular hypertrophy (LVH). A population survey was performed in 1982-1985 and repeated in 1989-1992. During the second survey, subjects in the age range 40-60 years were invited to undergo an M-mode echocardiographic examination. A total of 487 subjects who participated in both surveys are included in the present analysis. Some of them (294) were normotensive (Group 1), 110 were hypertensive but had never taken antihypertensive drugs (Group 2), 47 hypertensives on drugs were in good BP control (Group 3) and 36 hypertensives on drugs had uncontrolled hypertension (Group 4). BP values at the 1989-1992 examination were, respectively, 122/77, 145/86, 124/78 and 153/91 mmHg, while 7 years earlier were 122/77, 133/84, 136/85 and 152/95 mmHg. Despite normal BP levels in Group 3, left ventricular mass index (LVMi, g/m(2.7)) was greater than in normotensives (42.4+/-10, 46.6+/-13, 47.0+/-10, 51.9+/-15 g/m(2.7)). Accordingly, the prevalence of LVH (LVMi >51 g/m(2.7)) was 18, 26.4, 36.7 and 50% in groups 1-4, respectively. The 193 hypertensives were, thereafter, divided according to BP control (ie <140/90 mmHg) on both surveys (1983-1985 and 1989-1992): 27 hypertensives with optimal BP levels on both visits also had a ventricular mass similar to normotensives and significantly lower than the other hypertensives (LVMi 44.6+/-11.6 vs 48.5+/-13.2, P<0.001). In conclusion, these findings indicate that hypertensive patients with BP values at levels similar to those in normotensives for a long period do not increase their left ventricular mass in comparison to subjects with normal BP levels.     

Ventricular arrhythmias in hypertensive left ventricular hypertrophy. Relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis

Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The relationships, however, between ventricular arrhythmias and coexistent coronary artery disease, left ventricular dysfunction and left ventricular fibrosis have not been examined in hypertensive LVH. We carried out coronary arteriography on fifteen hypertensive patients with LVH and nonsustained ventricular tachycardia (greater than or equal to 3 consecutive ventricular complexes) of whom nine (60%) were free of significant (greater than 50% stenosis) coronary disease. To identify other possible correlates of left ventricular arrhythmias, 28 patients with LVH, comprising 17 with ventricular tachycardia and 11 without ventricular arrhythmias, underwent quantitative assessment of left ventricular function (angiographic ejection fraction), left ventricular mass (echocardiography), and left ventricular fibrosis (endomyocardial biopsy). Ejection fraction was not significantly different between the two groups (53 +/- 8% v 62 +/- 2%, P = NS). However, left ventricular mass was significantly greater (442 +/- 28 g v 339 +/- 34 g, P less than .05) and percentage fibrosis significantly higher (19 +/- 4% v 3 +/- 1%, P less than .001) in those patients with ventricular tachycardia. Thus ventricular arrhythmias in hypertensive patients with LVH cannot be entirely attributed to coexistent coronary disease, nor to left ventricular dysfunction, but are related to the degree of cardiac hypertrophy and subendocardial fibrosis.     

Epicardial coronary artery size in hypertensive and physiologic left ventricular hypertrophy

BACKGROUND: In the hypertensive heart, epicardial arteries are not enlarged, despite increased total coronary flow related to augmented cardiac workload, wall stress, and left ventricular (LV) mass. The aims of this study were to assess the impact of different hemodynamic factors and LV mass on baseline left main coronary artery (LMA) size in hypertensive LV hypertrophy (LVH) and physiologic LVH, used as a pressure-independent model of hypertrophy. METHODS: In 104 subjects without coronary disease (26 normotensive subjects without LVH, 15 athletes with physiologic LVH, and 63 untreated hypertensive subjects [28 without and 35 with LVH]), LMA size and coronary flow reserve (CFR) were measured by transesophageal echocardiography, and LV mass, volumes, stroke work, and wall stress were measured by transthoracic echocardiography. RESULTS: The LMA area in normotensive control subjects, athletes, and hypertensive subjects without and with LVH was 13.2 +/- 4.2, 17.5 +/- 2.9, 10.1 +/- 3.2 and 13.1 +/- 3.9 mm(2). In normotensive control subjects, LMA size increased with body surface area, rate-pressure product, stroke work, and LV mass or wall thickness (r = 0.39, 0.39, 0.47 and 0.67 or 0.62, P < .05-0.01). In athletes with physiologic LVH, LMA area increased with CFR (0.65, P < .01). In the whole hypertensive population, LMA lumen increased with LV mass (r = 0.40, P < .01), and decreased with office systolic blood pressure (r = -0.48, P < .01). CONCLUSIONS: In the hypertensive LVH, baseline LMA area is not increased and is inversely related to office systolic blood pressure. In the physiologic LVH, increase in baseline LMA size seems to reflect effect of high-flow stimuli.     

QT dispersion intervals in hypertensives with left ventricular hypertrophy

Left ventricular hypertrophy is an important risk factor of cardiovascular complications during the course of hypertension. Increased QT dispersion is associated with sudden cardiac death in congestive heart failure and in other cardiovascular diseases. Our aim was to compare QT dispersion from routine ECG in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Authors examined 71 hypertensives treated in our medical department. Left ventricular hypertrophy was defined by echocardiography (Penn convention) as left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women. QT dispersion was defined from routine ECG (QTmax - QTmin). Presence of LVH was found in 26 patients (mean age 59.3 years), absence of LVH in 45 patients (mean age 57.8 years). Hypertensives with secondary hypertension, hypertrophic cardiomyopathy, sings of ischemia in ECG, arrhythmias, myocardial infarction, heart failure, diabetes mellitus and patients treated by antiarrhythmic drugs of the Ic and III groups were excluded. Both groups of hypertensives were matched by demographic parameters, and by the presence of hypertension, obesity, hyperlipidemia and smoking habites. There were statistically significant longer QT dispersion and QTc dispersion (59.0 +/- 20.1 ms, 64.0 +/- 23.7 ms) in LVH-positive patients than in LVH-negative once (43.2 +/- 9.5 ms, 48.4 +/- 11.1 ms). Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease. Authors recommend to look after left ventricular hypertrophy presence in hypertensives as it carries much more complicated course of the disease. Measurment of QT dispersion adds farther stratificational information to these patients.     

Influence of exercise on QT dispersion in hypertensive patients with left ventricular hypertrophy without coronary artery disease

In hypertensive patients with left ventricular hypertrophy (LVH), the influence of exercise on the regional variations in ventricular repolarization is not well understood. The present study compared dispersions of QT and QT apex (QTD and QTaD), which are indices of regional variations in ventricular repolarization, between hypertensive patients with echocardiographic evidence of LVH and those without LVH. Seventy essential hypertensive patients underwent a modified Bruce protocol exercise test, and QTD and QTaD were measured at rest and at peak exercise level. All subjects had undergone coronary angiography and did not have coronary artery disease. None of them showed ST-segment depression during or after exercise. There were 20 patients with LVH and 50 patients without LVH. The QTD and QTaD at rest were not different between the patients with LVH and those without LVH (56+/-32 vs 57+/-28 ms, 52+/-20 vs 49+/-23 ms). At peak exercise level, QTaD was significantly decreased compared with the baseline in hypertensive patients without LVH (49+/-23 to 42+/-16ms, p<0.05), whereas in patients with LVH QTaD increased (52+/-20 to 67+/-17ms, p<0.05). QTaD at peak exercise level was positively correlated with the left ventricular mass index (r=0.357, p=0.0024). These data were unchanged after correction for heart rate using Bazett's equation. In conclusion, QTaD increased after exercise in hypertensive patients with LVH. Inhomogeneity of repolarization is induced by exercise stress in hypertensives with LVH.     

Left ventricular diastolic function in athletes and borderline hypertensives with mild cardiac hypertrophy.

The aim of this study was to evaluate the diastolic function in athletes and in young borderline hypertensives with mild left ventricular hypertrophy. Left ventricular filling was assessed by echo Doppler measurement of transmitral flow velocity in 18 soccer players (age 22 +/- 4 years, left ventricular mass index, LVMI 136 +/- 12 g/m2), in 15 borderline hypertensives (age 21 +/- 3 years, LVMI 137 +/- 9 g/m2), and 20 normotensive subjects (age 22 +/- 4 years, LVMI 93 +/- 10 g/m2) as reference group. We found that left ventricular filling profile was similar in borderline hypertensives, in athletes and in normotensive subjects. These findings suggest that, at least in the early stage, mild cardiac hypertrophy secondary to borderline blood pressure elevation is characterized by indexes of diastolic function not different from those found in athletes with physiological hypertrophy.     

Abnormal ventricular repolarization in hypertensive patients: role of sympatho-vagal imbalance and left ventricular hypertrophy

BACKGROUND: An increased risk for life-threatening arrhythmias and sudden death has been observed in hypertensive patients, associated with either left ventricular hypertrophy (LVH) or prolonged QT interval. To investigate the influence of autonomic imbalance and LVH on QT interval in hypertensive patients, we compared two different models of LVH: hypertension and endurance physical training. METHODS: Forty-seven untreated subjects affected by essential hypertension and 35 endurance runners, with a similar degree of LVH, were enrolled into the study. All subjects underwent 24-h ambulatory ECG recording and morning blood sampling for catecholamines. Heart rate variability was evaluated by spectral analysis and a computerized algorithm was used to measure the QT interval; QTc was then computed by the Bazett's formula. Left ventricular mass index (LVMI) was assessed by echocardiogram. RESULTS: No difference in LVMI was found between hypertensive patients and athletes. Athletes showed lower heart rate (64 +/- 1 vs. 75 +/- 1 bpm, p<0.001, mean +/- S.E.M.) and shorter QTc (401 +/- 3 vs. 434 +/- 4 ms, p<0.001) than hypertensive patients throughout the 24-h period. Athletes showed a higher vagal drive compared to hypertensive patients as suggested by bradycardia and higher values of vagal indices, which negatively correlated with QTc. Plasma norepinephrine was significantly lower in athletes than in hypertensive patients (p<0.05) and positively correlated with QTc. Conclusion: Despite similar degrees of LVH, hypertensive patients show QTc lengthening, as compared to athletes. Heart rate variability and plasma norepinephrine levels suggest sympathetic predominance in hypertensive patients, which could contribute to abnormal ventricular repolarization, thus identifying patients with an increased arrhythmic risk.     

QTc dispersion and complex ventricular arrhythmias in untreated newly presenting hypertensive patients.

Increased dispersion of ventricular repolarisation (increased QT dispersion) is believed to predispose to arrhythmias associated with sudden death in certain cardiac diseases. Hypertension is also associated with increased risk of sudden death, particularly in those with left ventricular hypertrophy (LVH). Therefore, the first aim of this study is to look into the possible pathogenic role of QT dispersion on the ventricular arrhythmias occurring in a group of never-treated hypertensive patients. The second aim is to look at other possible determinants of QT dispersion (ie, level of blood pressure, hypokalaemia, electrocardiographic LVH and presence or absence of strain pattern) in hypertensive patients, and their relevance to complex ventricular arrhythmias. QTc (corrected QT) was measured in 70 newly presenting (never-treated) hypertensive patients (47 male, 23 female, mean age 51.9 +/- 12.5 years) from a standard 12-lead surface electrocardiogram (ECG). Blood pressure measurements and 24-h ECG holter recordings were performed in all patients. Serum potassium level was measured in 51 of the patients. Ventricular arrhythmias were classified using a modified Lown's scoring system. Maximum QTc, minimum QTc and QTc dispersion for all patients were 442 +/- 30.3 ms, 380 +/- 26.7 ms and 61.5 +/- 21.6 ms respectively. High grade ventricular arrhythmias (Lown's score >/=3) were found in 43% of the patients. The QTc dispersion was strongly correlated with the Lown's classification of arrhythmia and the age of the patients. Patients with more severe ectopy (Lown's score >/=3) were significantly older (57.4 +/- 10.3 years) compared to those with score /=3 Lown's score compared to 39% in the group with LVH but without strain. In the presence of relative hypokalaemia, hypertensive patients with LVH showed more QTc dispersion (85.7 +/- 15.5 ms) and a greater tendency for complex ventricular arrhythmias (100% grade >/=3 Lown's score) compared to those with LVH and normal serum potassium levels (64.1 +/- 22.6 ms and 35%, QTc dispersion and Lown's score >/=3, respectively P = 0. 05). The level of blood pressure had no effect on either the QTc dispersion or the prevalence of complex ventricular arrhythmias. Prevalence of complex ventricular arrhythmias in hypertensive patients is strongly correlated with QTc dispersion and age. When hypertensive patients with LVH have low potassium levels the risk of developing complex ventricular arrhythmias is significantly increased.     

Diminished nocturnal decline in blood pressure in elderly hypertensive patients with left ventricular hypertrophy.

To assess the circadian blood pressure (BP) changes in elderly hypertensive patients with left ventricular hypertrophy (LVH), the ambulatory BP was measured noninvasively every 30 minutes for 24 hours in those patients with LVH (n = 15) and without LVH (n = 23), and in normotensive elderly subjects (n = 11). Although the daytime systolic BP (SBP) was comparable in the two hypertensive groups, the nighttime SBP in patients with LVH tended to be higher than in patients without LVH (149.0 +/- 15.1 versus 138.4 +/- 20.1 mm Hg, p less than 0.10). The LV mass index correlated significantly with the nighttime SBP (r = 0.43, p less than 0.01), but not with the daytime SBP (r = 0.24, ns), with clinic SBP (r = 0.14, p = ns) or the SBP after handgrip exercise (r = 0.31, p = ns). The difference in the systolic BP between daytime and nighttime (D-N SBP) in patients with LVH (2.8 +/- 9.4 mm Hg) was significantly less than that in patients without LVH (12.8 +/- 16.0 mm Hg) (p less than 0.02). In addition, the D-N SBP correlated inversely with the left ventricular mass index (r = -0.33, p less than 0.05). It was concluded that hypertension in the elderly with LVH was associated with a diminished nocturnal decline in blood pressure.     

Left ventricular hypertrophy is associated with an attenuated endothelium-dependent vasodilation in hypertensive men

To investigate the relationship between left ventricular hypertrophy (LVH) and endothelium-dependent vasodilation (EDV), 30 untreated hypertensive patients, 18 treated hypertensives (53 +/- 7 years, all males) and 26 age-and sex-matched healthy normotensive controls, underwent evaluation of EDV and endothelium-independent vasodilation (EIDV) in the forearm, by means of local intra-arterial infusions of methacholine (MCh, evaluating EDV) and sodium nitroprusside (SNP, evaluating EIDV). Forearm blood flow was measured by venous occlusion plethysmography and LVH was measured by echocardiography. The reduction in forearm vascular resistance during MCh infusion (4 microg/min) was significantly smaller in the hypertensive patients with LVH when compared to those without LVH, both in the untreated (-61 +/- 12%, n = 19 vs -72 +/- 4%, n = 11, p < 0.01) and in the treated group (-60 +/- 15%, n = 11 vs -75 +/- 5%, n = 7, p < 0.01). Thereby, EDV was significantly impaired only in the hypertensive patients with LVH when compared to controls (-77 +/- 7% at MCh 4 microg/min, p < 0.001). EIDV was not significantly different between patients with and without LVH and controls. In conclusion, the presence of LVH was related to endothelial dysfunction, both in untreated and treated hypertensive patients, suggesting either a role for endothelial function in the development of LVH, or that a dysfunctional endothelium and LVH are coexisting markers of a more severe hypertensive disease.     

Effects of angiotensin II receptor blockade-based therapy with losartan on left ventricular hypertrophy and geometry in previously treated hypertensive patients

BACKGROUND: The 2003 European Society of Hypertension/European Society of Cardiology (ESH/ESC) guidelines recommend angiotensin II receptor antagonists (AIIRAs) as a first-line therapy in hypertensives with left ventricular hypertrophy (LVH). AIM: We investigated the long-term effects of an AIIRA-based therapy on left ventricular (LV) structure and geometry in previously, unsatisfactorily treated essential hypertensive patients. METHODS: Sixty-eight consecutive patients referred to our hypertension hospital outpatient clinic with: (i) LVH (LV mass index, LVMI 51 g/m(2.7) in men and 47 g/m(2.7) in women), (ii) uncontrolled clinic blood pressure (BP140 and/or 90 mmHg) and (iii) antihypertensive therapy not including angiotensin-converting enzyme (ACE) inhibitors or AIIRAs were selected for this study. Two-dimensionally guided M-mode echocardiograms were carried out at baseline and after 6, 12, 18 and 24 months of follow-up. In all patients, losartan (50-100 mg/day, mean dose 82 mg/day) was added as first step to the previous therapy. Additional drugs, tailored to the single patient, were added, if necessary, to achieve target BP values (<140/90 mmHg). RESULTS: Overall, 59 patients completed the study with the primary efficacy measurements (LVMI) at all appropriate times. A significant reduction in both clinic systolic BP and diastolic BP was found across the entire period of study respect to baseline (-17/10, -22/12, -24/13 and -26/14 mmHg at 6, 12, 18 and 24 months, p < 0.001 respectively), leading to target clinic BP in 75.6% of cases. LVMI was significantly lower after 1 year of treatment (-11 +/- 12%, p < 0.05) with a further significant reduction at the end of treatment (-22 +/- 18%, p < 0.01). The proportion of patients achieving normalization of LVMI was 47.4% and more importantly, the prevalence of concentric LVH fell from 38.9% to 6.7% (p < 0.01). CONCLUSIONS: Our findings indicate that long-term intensive treatment based on the AIIRA losartan induced a normalization of LVH in about 50% of patients and more importantly caused an almost complete regression of concentric LVH, the most dangerous adaptive pattern. The transition from concentric to normal or eccentric LV geometry may have in these high-risk patients a favourable prognostic implication in addition to the recognized positive effect of reducing LVMI.     

Difference in coronary blood flow dynamics between patients with hypertension and those with hypertrophic cardiomyopathy.

We studied twelve patients with hypertensive left ventricular hypertrophy (LVH), 10 patients with hypertrophic cardiomyopathy (HCM) and 10 control subjects to examine the differences in coronary blood flow (CBF) dynamics between patients with hypertensive LVH and those with HCM. All subjects had normal coronary arteriograms. Measurements of CBF using Doppler Flo-Wire were performed at rest, and after infusions of acetylcholine and papaverine. The baseline CBF was significantly increased in both hypertensive LVH patients and HCM patients compared to that noted in control subjects (64.1+/-36.9, 80.0+/-38.1, 32.3+/-8.0 ml/min, respectively, p<0.01). Coronary flow reserve and endothelium-dependent vasodilatation were significantly lower in hypertensive LVH patients and HCM patients than in control subjects, but there was no significant difference between the hypertensive LVH and HCM patients themselves. In contrast, the diastolic/systolic velocity ratio at baseline was significantly lower in hypertensive LVH patients than in HCM patients (1.53+/-0.40, 6.31+/-7.50, p<0.05). Although CBF and coronary flow reserve correlated positively and negatively, respectively, with left ventricular mass index (r=0.51, -0.59, respectively), the diastolic/systolic velocity ratio at baseline did not show a significant correlation to left ventricular mass index. In conclusion, the diastolic/systolic velocity ratio differed between hypertensive LVH and HCM patients, independent of left ventricular mass. These results suggest that the difference of phasic pattern of CBF may be essential for coronary circulation in patients with hypertensive LVH and in those with HCM.     

Assessment of self-monitoring of blood pressure in the diagnosis of isolated clinic hypertension

BACKGROUND: There are no studies assessing cardiovascular morbidity, morality in patients with isolated clinical hypertension (ICH) with self-blood pressure monitoring (SBPM). OBJECTIVES: To determine the value of SBPM in the diagnosis of ICH. METHODS: Cohort study. New hypertensive and normotensive patients 15-75 years, without cardiovascular events history. VARIABLES: Oriented anamnesis hypertension; blood pressure measurements (BP): clinical BP, SBPM and ambulatory BP monitoring (ABPM); evaluation of target organ damage (TOD); electrocardiogram; retinography and microalbuminuria (MA). RESULTS: One hundred and thirty-five patients, 95 hypertensive (62.1% males; mean age 59.08+/-16.8 years), 40 normotensive (37.5% males; mean are 56.32+/-10.22 years). BP measurements (mmHG) in normotensives vs hypertensives: clinical BP, 125.36/76.74 vs 149.81/87.86 mmHg (p<0.0001) and SPPM, 114.90/69.96 vs 142.06/86.31 (p<0.0001). Twenty-four-hour ABPM: 135.41/81/81.74. Prevalence of TOD in hypertensive: 23.10% left ventricular hypertrophy (LVH), sustained hypertension (SH): clinic BP, 149.88/86.34 vs 152.51/89.55 (p>0.10); SBPM: 147.895/88.95 vs 128.17/79 (p<0.0001) and ABPM, 141.72/88.22 vs 131.66/80 (p=0.053 for systolic). TOD in SH vs ICH: LVH, 24.6% vs 19.2% (p=0.814); exudates or haemorrhages, 7.7% vs 9.8% (p=0.580). The risk of an occurrence of any TOD in ICH patients is lower for 125/80 (OR=2.5). CONCLUSIONS: VAMPAHICA will provide information about value SBPM in the diagnosis of ICH. Advanced retinopathy is relative frequent in ICH patients. If TOD is accepted as a surrogate endpoint, the diagnostic values of ICH will be probably decreased.     

Effect of cilnidipine on left ventricular function in hypertensive patients as assessed by tissue Doppler Tei index

Tissue Doppler Tei index is pointed to be more effective in the evaluation of global cardiac function than systolic and diastolic measurements alone in various heart diseases. This study was designed to assess the effect of cilnidipine on left ventricular function in hypertensive patients by using this index. A group of 40 hypertensives (mean age 55+/-8 years, range: 35-65) and 16 controls (mean age 52+/-9 years, range: 36-65) were included. Hypertensives were classified into non-left ventricular hypertrophy (NLVH) group (25 patients) and left ventricular hypertrophy (LVH) group (15 patients), and treated with cilnidipine for 2 months. Before and after treatment, the participants were examined by echocardiography. Tissue Doppler Tei index was calculated as diastolic time interval measured from end of late diastole to origin of early diastole (a') minus systolic Sm duration (b') divided by b', that is Tei index = (a'-b')/b'. Thirty-seven hypertensive patients finished the treatment. Tei index was significantly higher in NLVH and LVH groups than in control group, and in LVH group than in NLVH group (0.44+/-0.07 vs 0.28+/-0.06, P < 0.001; 0.51+/-0.13 vs 0.28+/-0.06, P < 0.001; 0.51+/-0.13 vs 0.44+/-0.07, P < 0.05). After treatment, Tei index was significantly decreased (0.40+/-0.11 vs 0.46+/-0.10, P < 0.0001); systolic blood pressure and diastolic blood pressure were also decreased significantly. In conclusion, Tei index is impaired in hypertensives before development of ventricular hypertrophy and impairment is more prominent in hypertrophy. Cilnidipine can improve left ventricular function. Tissue Doppler Tei index is gaining importance in evaluating LV function after drug intervention in hypertensive patients.     

Patterns of QT Dispersion in Athletic and Hypertensive Left Ventricular Hypertrophy

Objective: The objective of this article is to assess whether left ventricular hypertrophy (LVH) due to physical training or of hypertensive patients shows similarities in QT length and QT dispersion. Methods: A total of 51 subjects were studied: 17 essential hypertensive patients (27.7 ± 5.6 years), 17 athletes involved in agonistic activity (canoeing) (24.8 ± 6.1 years), and 17 normotensive healthy subjects as control group (24.8 ± 3.6 years). The testing protocol consisted of (1) clinic BP measurement, (2) echocardiography, (3) 12‐lead electrocardiographic examination (QT max, QTc max, QT min, QTc min, ΔQT, ΔQTc). Results: There were no significant differences between the body surface area, height, and age of the three groups. Clinic blood pressure was higher in hypertensives (146.5 ± 45.2/93.5 ± 4.9 mmHg) versus athletes (120.9 ± 10.8/77.1 ± 6.0 mmHg) and controls (123.5 ± 4.8/78.8 ± 2.9 mmHg) by definition. Indexed left ventricular mass (LVM/BSA) was significantly greater in both athletes (148.9 ± 21.1 g/m²) and hypertensives (117.1 ± 15.2 g/m²) versus controls (81.1 ± 14.5 g/m²; P < 0.01), there being no statistical difference among them. LVH (LVMI > 125 g/m²) was observed in all athletes, while the prevalence in hypertensives was 50%. In spite of this large difference in cardiac structure there were no significant differences in QT parameters between athletes and the control group, while hypertensive patients showed a significant increase in QT dispersion versus the two other groups (ΔQT 82 ± 2.1, 48 ± 1.3, 49 ± 2.3 ms; P < 0.01; ΔQTc 88 ± 2.0, 47 ± 1.4, 54 ± 2.7; P < 0.01). Conclusions: LVH induced by physical training activity is not associated with an increase in QT dispersion, whereas pathological increase in LVM secondary to hypertension is accompanied by an increased QT dispersion.     

Determinants of left ventricular hypertrophy in arterial hypertension

A long term study (2-7 years, mean 3.6 years) monitoring 112 clinical and echocardiographic pattern in 593 hypertensives and 156 normotensives was performed in order to find associations to left ventricular hypertrophy (LVH) developing later. 49% of the hypertensives developed echocardiographic signs of LVH (wall thickness of 12 mm and more), in contrast to 5.1% of normotensive persons. Multivariate analysis revealed the following parameters examined at entry were associated with LVH on follow-up: male sex, prolonged hypertensive history, higher diastolic blood pressure, frequent lipid-metabolism disturbances, uncharacteristic chest pain and less effective antihypertensive treatment. Thus, LVH development can be regarded as a multifactorial process.     

Heart failure in hypertensive patients with left ventricular hypertrophy

Left ventricular hypertrophy (LVH) is supposed to be a useful marker of cardiovascular complications during the course of hypertension. Authors compared the presence of heart failure, left ventricular diastolic dysfunction and chronic atrial fibrillation in hypertensive patients with and without left ventricular hypertrophy defined by echocardiography. Hospital records of 192 hypertensives treated in our medical department during years 1996-1999 were analysed. Left ventricular hypertrophy was defined by echocardiography (Penn convention) as left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women. Presence of LVH was found in 128 patients (mean age 65.9 years), absence of LVH in 64 patients (mean age 64.8 years). Both groups of hypertensives were matched by demographic parameters, by the presence of hyperlipidemia, by smoking habits. Hypertensive patients with left ventricular hypertrophy were more often treated by ACE inhibitors. There were statistically significant more patients with heart failure, left ventricular diastolic dysfunction and chronic atrial fibrillation in LVH-positive patients than in LVH-negative once. There was also statistically significant lower ejection fraction (50.3 +/- 11.4% vs 56.5 +/- 7.4%) in LVH-positive patients than in LVH-negative once. Left ventricular hypertrophy in patients with hypertension brings usually a complicated course of the disease with a high contribution to the development of chronic heart failure.     

Left ventricular hypertrophy in patients with autonomic failure

BACKGROUND: In autonomic failure (AF), supine hypertension may predispose patients to end-organ damage. The pathophysiology of hypertensive heart disease in AF is not known. The aim of the present study was to evaluate the prevalence and predisposing factors of left ventricular hypertrophy (LVH) in patients with AF. METHODS: We studied 25 patients with AF (67 +/- 8 years); 80% were being treated for orthostatic hypotension. Twenty patients with essential hypertension (68 +/- 6 years) were considered as the control group. All subjects underwent echocardiography for measurement of left ventricular mass (LVM). The patients with AF underwent a 24-h BP monitoring and long-term blood pressure (BP) variability was calculated as standard deviation (SD) of the average of the half-hour mean values. RESULTS: The LVM is comparable in patients with AF and hypertensive controls (145 +/- 35 g/m2 v 127 +/- 32 g/m2, P = .07). The proportion of patients with LVH is similar in both populations (AF 80%, hypertensive 70%). The patients with AF were divided into two groups, with and without LVH. The SDs are significantly higher in AF patients with LVH than in those with normal LVM (SD 24-h systolic BP: 22 +/- 4 v 14 +/- 1 mm Hg, P = .001). CONCLUSIONS: A high proportion of patients with AF show LVH. The LVM values are comparable with those of patients with essential hypertension. The development of LVH seems to depend on high BP variability, characteristic of AF patients. Detection of LVH may help in the choice of treatment for orthostatic hypotension and in the prevention of heart failure.     

Losartan reduces left ventricular hypertrophy proportionally to blood pressure reduction in hypertensives, but does not affect diastolic cardiac function

In contrast to the well-recognized salutary effects of angiotensin-converting enzyme inhibition, the value of angiotensin II type I (ATl)-receptor blockade on left ventricular hypertrophy (LVH) is controversial. In addition, the data on the influence of this therapy on cardiac diastolic function are scarce. Thirty-nine patients with moderate primary hypertension, LVH, and normal systolic function received losartan, 50 to 100 mg daily. Transthoracic echocardiography was performed at baseline and after 6 months of treatment. Thirty-one patients completed and were included in the study (16 males, 61.1 +/- 1.0 years). The patients were divided into responders if mean blood pressure (BP) decreased > 5 mm Hg at the end of the study (20 patients) and non-responders (mean BP decrease < or = 5 mm Hg, 11 patients). The BP and the LVH were significantly reduced (systolic BP by 10.0%, diastolic BP 6.5%, mean BP 8.2%, left ventricular mass index [LVMI] 6.2%, interventricular septum 5.8%, posterior wall 3.0%) (p< or =0.02), attributed to the reduction of BP and LVH in responders; the LVH in non-responders did not alter with treatment. A significant correlation was noted between changes in BP and LVMI (r=0.60, p<0.001). The systolic cardiac function remained normal. The Doppler parameters usually used to assess the diastolic function of the LV (early diastolic filling velocity [E wave], late diastolic filling velocity [A wave], ratio of E/A waves, isovolumic relaxation time), which were abnormal at baseline, did not change with treatment. The size of the left atrium increased (p<0.05) at the end of the study. In conclusion, a 6-month course with losartan decreased BP and LVH. However, the LVH regression was rather associated with the reduction of the hemodynamic stimulus per se, than any trophic effect of the drug in the myocardium. The diastolic cardiac function remained abnormal with treatment.     

Coronary flow velocity reserve is diminished in hypertensive left ventricular hypertrophy

BACKGROUND: Dipyridamole stress transesophageal echocardiography (STEE) is a feasible method for the evaluation of coronary flow velocity reserve (CFR). AIM: The aim of the present study was to investigate CFR in hypertensive patients with or without left ventricular hypertrophy (LVH). METHODS: The study comprised 73 patients with a negative coronary angiogram (29 men and 44 women). Three different groups were compared: normotensive patients, hypertensive patients without LVH and hypertensive patients with LVH. RESULTS: CFR was significantly decreased in patients with hypertension with LVH as compared to normotensive cases (2.19+/-0.50 vs 2.71+/-1.10; p<0.05). CFR of hypertensive patients without LVH was only slightly reduced as compared to normotensive cases (2.44+/-0.81 vs 2.71+/-1.10; p=ns). In hypertensive patients with LVH, the LV mass and LV mass index were inversely related to CFR (r = -0.481 and -0.477, p<0.05, respectively). CONCLUSIONS: CFR is diminished in patients with hypertension. The degree of CFR reduction is related to the extent of LVH.