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PubMed2003

Does a prolonged QT peak identify left ventricular hypertrophy in hypertension?

BACKGROUND: Left ventricular hypertrophy is a powerful predictor of death. Hypertensive subjects with left ventricular hypertrophy can have increased QT (end) dispersion, which is associated with cardiac death. Despite its prognostic value, QT (end) dispersion is not widely used. QTp (i.e. start of QRS to peak of T wave) is easier to measure. Therefore, we tested the hypothesis that long QT peak was associated with left ventricular hypertrophy and assessed its cost-effectiveness at diagnosing left ventricular hypertrophy. METHODS: ECGs and echocardiograms were recorded in 47 hypertensive patients. The onset of the QRS complex and peak of T wave of lead I of each subject's ECGs were digitised by one observer blind to results of the echocardiogram. Receiver-operator characteristics curves were plotted to determine the sensitivity and specificity of different cut-off values of QT peak at predicting left ventricular hypertrophy (defined as left ventricular mass index> or =134 g/m2 in male, > or =110 g/m2 in female). RESULTS: The heart-rate corrected QT peak of lead I correlated with left ventricular mass index (r=0.45, P=0.002). If all patients with a prolonged QT peak (> or =300 ms) had an echocardiogram, then no cases of left ventricular hypertrophy would be missed (100% sensitive). This novel ECG criterion not only had better positive and negative predictive values than the Sokolow-Lyon voltage criteria, but also resulted in more cost-effective resource use (< pound 370 vs. pound 1750/case of left ventricular hypertrophy detected). CONCLUSION: If the results of this small pilot study are confirmed in larger studies, then measuring QT peak of lead I may become a cost-effective way of identifying hypertensives who are likely to have echocardiographic left ventricular hypertrophy.

Adult↗
PubMed1997

Diltiazem slow-release and left-ventricular hypertrophy: a volumetric approach of left ventricular mass using magnetic resonance imaging.

AIMS: This study was designed to assess the changes in left ventricular mass (LVM) in hypertensive patients with left ventricular hypertrophy under drug therapy with once-daily slow-release diltiazem. Magnetic resonance imaging (MRI) was used for this purpose because of its higher reproducibility than M-mode or two-dimensional echocardiography. METHODS: Patients suffering from essential hypertension were included if their baseline LVM index (LVMI) was > or = 105 g/m2 in male or > or = 85 g/m2 in female patients, ie, equal or higher to the median values observed in hypertensive patients in our institution. MRI consisted in a true short-axis, electrocardiogram (ECG) gated spin-echo slice acquisition at baseline, after 3 and 6 months of therapy (M0, M3, and M6). Data were stored on magnetic tapes and read subsequently under blind conditions and the control of an external auditor. RESULTS: Thirty-five patients were included. Of these, 14 patients (40%) were not previously treated. Inter- and intra-observer variability for LVMI measurement were 5.6 +/- 4.3% and 2.1 +/- 3.0%, respectively. Mean baseline LVMI was 110 +/- 16 g/m2 in male and 96 +/- 16 g/m2 in female patients. It decreased by 3.6% at M3 (P = 0.05) and by 6.0% at M6 (P = 0.02). A trend towards a greater LVMI reduction was observed in previously untreated patients. CONCLUSION: This study confirms that MRI is a reproducible technique for the measurement of LVM. It demonstrates a significant reduction in LVMI as early as the 3rd month of therapy in hypertensive patients treated with once-daily sustained release (SR) diltiazem, although baseline LVMI in the majority of participating patients was only moderately increased.

Adult↗
PubMed2004

Regression of electrocardiographic left ventricular hypertrophy predicts regression of echocardiographic left ventricular mass: the LIFE study.

The electrocardiogram (ECG) is widely used for detection of left ventricular hypertrophy (LVH). However, whether changes in ECG LVH during antihypertensive therapy predict changes in LV mass remains unclear. Baseline and year-1 ECGs and echocardiograms were assessed in 584 hypertensive patients with ECG LVH by Sokolow-Lyon or Cornell voltage-duration product criteria at entry into the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiographic substudy. A >/=25% decrease in Cornell product defined regression of ECG LVH; a <25% decrease defined no significant regression; and an increase defined progression of ECG LVH. Regression of echocardiographic LVH was defined by a >/=20% reduction in LV mass. After 1 year of therapy, 155 patients (27%) had regression of ECG LVH, 286 (49%) had no significant change, and 143 (25%) had progression of ECG LVH. Compared with patients with progression of ECG LVH, patients with no significant decrease and patients with regression of ECG LVH had stepwise greater absolute decreases in LV mass (-16+/-33 vs -29+/-37 vs -32+/-41 g, P<0.001), greater percent reductions in LV mass (-5.7+/-14.6 vs -11.3+/-13.6 vs -12.3+/-15.6%, P<0.001), and were more likely to decrease LV mass by >/=20% (11.2 vs 24.8 vs 36.1%, P<0.001), even after adjusting for possible effects of baseline and change in systolic and diastolic pressures. Compared with progression of ECG LVH, regression of the Cornell product ECG LVH is associated with greater reduction in LV mass and a greater likelihood of regression of anatomic LVH.

Aged↗
PubMed1990

Electrocardiographic diagnosis of left ventricular hypertrophy in the presence of left bundle branch block: a wasted effort.

We assessed the reliability of multiple electrocardiographic variables for detecting left ventricular hypertrophy in 100 patients (aged 23 to 92 years, mean age 39 +/- 14) with complete left bundle branch block and different underlying cardiac diseases. Left ventricular hypertrophy, defined as an echocardiographically evaluated left ventricular mass greater than 241 g, was present in 66 of the 100 patients. The electrocardiographic parameters with the highest sensitivity were both the Cornell voltage criteria (RaVL + SV3 greater than 28 mm in men and greater than 20 mm in women) and the combination of criteria proposed by Kafka (any of these four indexes: RaVL greater than or equal to 11 mm, QRS axis -40 degrees or less, SV1 + RV5 or RV6 greater than or equal to 40 mm, SV2 greater than or equal to 30 mm and SV3 greater than or equal to 25 mm), with a sensitivity of 77%. Both criteria had a very low specificity (32 and 35%, respectively). The high specificities (greater than or equal to 88%) of several electrocardiographic criteria were accompanied by ineffective low sensitivities (less than 35%). Moreover, the cumulative parameters of Kafka and Cornell voltage criteria achieved a sensitivity of 84 and 89%, respectively, in hypertensive patients and in those with valvar diseases. None of the electrocardiographic indexes tested showed a significant difference in sensitivity when applied in categories of patients with left ventricular hypertrophy and different left ventricular geometry (cavity dilation or concentric hypertrophy). These data indicate that both conventional and recently proposed electrocardiographic criteria for left ventricular hypertrophy in the presence of left bundle branch block poorly recognize an augmented left ventricular mass.

Adult↗
PubMed1998

Power spectral analysis of the heart rate in hypertensive patients with and without left ventricular hypertrophy: the effect of a left ventricular mass reduction.

OBJECTIVE: The aim of this study was to evaluate the spectral analysis of the heart rate in normotensive subjects and in hypertensive patients with and without left ventricular hypertrophy (LVH), under basal conditions and after a reduction in left ventricular mass. SUBJECTS AND METHODS: In 12 normotensive subjects and 22 hypertensive patients (14 with and eight without LVH), we performed 24 h electrocardiogram Holter monitoring, ambulatory blood pressure monitoring and an echocardiographic study. Sequences of 512 R-R intervals, during daytime, afternoon and night-time periods, were taken for an evaluation of spectral analysis (Box-Jenkins method). We then calculated the absolute and percentage power spectral density of the peak centred at 0.10 Hz (low-frequency peak) and at 0.25 Hz (high-frequency peak). RESULTS: At baseline, a daytime to night-time decrease in the low-frequency peak was detected in normotensives (P < 0.01) and in hypertensives without LVH (P < 0.01), while no change was observed in hypertensives with LVH. The power spectral density low-frequency peak during the daytime and night-time was significantly greater in hypertensives with LVH than in those without LVH (P < 0.001) and in normotensive subjects (P < 0.001). Fourteen of these patients with LVH were given effective long-term antihypertensive treatment and were studied again 20 days after the treatment had been withdrawn, when blood pressure had increased to pretreatment values. In eight patients showing a reduction in LVH, we found a significant decrease in the power spectral density low-frequency peak and an increase in the high-frequency peak during daytime and night-time in respect to basal conditions, and circadian variations in the spectral indices of heart rate variability were restored. In contrast, in six patients without reversal of LVH, the power spectral density low-frequency peak did not change in respect to basal conditions and remained significantly higher in comparison with the patients with LVH regression. CONCLUSION: A reduction in LVH may be associated with restoration of daytime to night-time cardiac autonomic control, as evaluated by a power spectral analysis of the heart rate.

Adolescent↗
PubMedDate not supplied

Experimental aortic stenosis and corresponding left ventricular hypertrophy in sheep.

Left ventricular hypertrophy (LVH) is an independent cardiac risk factor. A simple standard experimental model of inducing LVH for further studies using experimental aortic stenosis in sheep was performed. The aim of this study is to describe animal-specific requirements as well as perioperative therapy, postoperative care, and the use of echocardiography for routine follow-up examinations. Supracoronary aortic banding was performed in 55 female sheep at an age of 6 to 8 months. General anesthesia and an antero-lateral thoracotomy were used. The objective was to achieve pressure gradients of 20 to 30 mm Hg. In addition a 4th intercostal space rib window was created to improve echocardiographic vision. The operations were completed successfully in all animals. Intraoperatively, little severe arrhythmia occurred. During the follow-up interval of 8 +/- 1.3 months, 8 animals died, due to incomplete perforation of the ascending aorta (3), chronic heart failure (2), pericardial cyst (1), and respiratory failure and infection (2). All remaining animals were amenable for further studies. Severe LVH was diagnosed with routine echocardiography on follow-up. Thus, experimental aortic stenosis in sheep is a safe and relatively simple technique to generate stable LVH. Echocardiography is an easy tool for follow-up evaluations. Due to low complication rates, the sheep model is well suited for further research in LVH.

Animals↗
PubMed1998

Time-voltage QRS area of the 12-lead electrocardiogram: detection of left ventricular hypertrophy.

Identification of left ventricular hypertrophy (LVH) using 12-lead ECG criteria based primarily on QRS amplitudes has been limited by poor sensitivity at acceptable levels of specificity. Because the product of QRS voltage and duration, as an approximation of the time-voltage area of the QRS complex, can improve accuracy of the 12-lead ECG for LVH, we examined the diagnostic value of true time-voltage area measurements of QRS complexes from the standard 12-lead ECG. Standard 12-lead ECGs and echocardiograms were obtained in 175 control subjects without LVH and in 74 patients with regurgitant valvular heart disease and LVH defined by echocardiographic criteria (indexed LV mass >110 g/m2 in women and >125 g/m2 in men). Standard voltage criteria, voltage-duration products (voltage multiplied by QRS duration), and true time-voltage areas of the QRS were calculated for Sokolow-Lyon criteria (SV1 +RV(5/6)) and the 12-lead sum of voltage criteria. Test sensitivities were compared using gender-specific partitions with matched specificity of 98% in the 175 subjects without LVH. Measurement of the time-voltage area significantly improved sensitivity for both criteria. The 76% sensitivity of the 12-lead sum area and 65% sensitivity of Sokolow-Lyon area were significantly greater than the 54% sensitivity of the approximation of QRS area provided by each voltage-duration product (P<.001 and P=.021) and than the 46% and 43% sensitivities of the respective simple voltage criteria (each P<.001). Comparison of receiver operating characteristic curves confirmed the superior overall performance of time-voltage area criteria compared with both voltage-duration products and simple voltage criteria. These results suggest that use of time-voltage areas can dramatically improve identification of LVH by 12-lead ECG. Further study of this approach is needed to identify optimal criteria for LVH based on the time-voltage area measurements from the 12-lead ECG.

Echocardiography↗
PubMed1995

Myocardial high-energy phosphate and substrate metabolism in swine with moderate left ventricular hypertrophy.

BACKGROUND: Although left ventricular hypertrophy (LVH) is frequently associated with impaired coronary vasodilator reserve, it is uncertain whether this leads to myocardial ischemia under physiological conditions. The goal of the present study was to determine whether swine with moderate LVH exhibit metabolic evidence of ischemia when myocardial oxygen requirements are increased. METHODS AND RESULTS: Myocardial metabolism was evaluated in an open-chest anesthetized preparation at baseline and during dobutamine infusion in 13 adolescent pigs with moderate LVH induced by supravalvular aortic banding and 12 age-matched control pigs. Transmural myocardial blood flow was quantified with radioactive microspheres; the ratio of phosphocreatine to ATP (PCr/ATP) in the anterior LV free wall was measured by 31P-nuclear magnetic resonance; and anterior wall lactate release was quantified from the arterial-coronary venous difference in 14C- or 13C-labeled lactate. In a subset of 5 animals from each group, the metabolic fate of exogenous glucose was determined from the transmyocardial difference in 6-14C-glucose and its metabolites 14C-lactate and 14CO2. Coronary reserve, as assessed by the ratio of blood flow during adenosine infusion to baseline blood flow, was significantly lower in the LVH pigs compared with controls (3.5 +/- 0.4 versus 5.5 +/- 0.4 mL/g.min, P < .05); however, transmural myocardial blood flow was similar in both groups of pigs, both at baseline and with dobutamine stimulation, probably reflecting the higher coronary perfusion pressure in the LVH pigs. At baseline, PCr/ATP tended to be lower in the LVH pigs (P = .09) but decreased similarly with dobutamine infusion in both groups. Isotopically measured anterior wall lactate release did not differ between the groups at baseline, nor did the increase in lactate release differ during dobutamine stimulation. The uptake of glucose, lactate, and free fatty acids did not differ between the groups in the basal state. However, during dobutamine stimulation, glucose uptake was greater in the LVH group (0.84 +/- 0.09 mumol/g.min versus 0.59 +/- 0.08 mumol/g.min, P < .05). In a subset of animals, 14C-glucose was used to assess glucose oxidation. These data showed that the LVH animals had a greater rate of glucose oxidation (0.6 +/- 0.10 versus 0.28 +/- 0.08 mumol/g.min, P < .05) and a greater rate of glucose conversion to lactate (0.20 +/- 0.04 versus 0.09 +/- 0.02 mumol/g.min, P < .05) compared with the control pigs. CONCLUSIONS: These results suggest that despite their reduced coronary vasodilator reserve and the absence of a greater rise in myocardial blood flow to compensate for a substantially higher LV double product, pigs with this model of moderate LVH do not exhibit a greater susceptibility to myocardial ischemia during dobutamine stress. However, LVH pigs exhibit significantly greater use of exogenous glucose during dobutamine stress, as evidenced by increases in both glucose oxidation and anaerobic glycolysis.

Adenosine Triphosphate↗
PubMed1997

[Regression of left ventricular hypertrophy in hypertensive patients].

Left ventricular hypertrophy associated with systemic hypertension differs from left ventricular hypertrophy initiated by other pressure overload diseases. Its development depends not only of hemodynamics aspects but of biochemical factors. Many studies have demonstrated a close link between left ventricular hypertrophy and cardiovascular morbidity and mortality. For that reason the idea of reversal of left ventricular hypertrophy has been a goal of the antihypertensive treatment. From the literature review has been established that the most classes of antihypertensive medications reduce the left ventricular mass, though there is a variation in required duration of treatment. At this point the angiotensin converting enzyme inhibitors, probably because a double effect: hypotensive and blockers of the trophic stimulus of angiotensin II, seemed to be the most potent for reducing the left ventricular mass. Still we don't know if reversal of left ventricular hypertrophy, by the antihypertensive treatment, reduce independently the cardiovascular risk.

Angiotensin II↗
PubMed2006

Association between electrocardiographic left ventricular hypertrophy with strain pattern and left ventricular structure and function.

BACKGROUND AND PURPOSE: Electrocardiographic left ventricular hypertrophy (LVH) with strain pattern has been documented as a marker for LVH. Its presence on the ECG of hypertensive patients is associated with poor prognosis. The study was carried out to assess the association of the electrocardiographic strain with left ventricular mass (LVM) and function in hypertensive Nigerians. MATERIAL AND METHODS: ECG as well as echocardiograms were performed in 64 hypertensive patients with ECG-LVH and strain pattern, 65 patients with ECG-LVH by Sokolow-Lyon (SL) voltage criteria and 62 normal controls. RESULTS: The study showed that electrocardiographic left ventricular (LV) strain pattern is associated with dilated left atrium, larger LV internal dimensions and greater absolute and indexed LVM in hypertensive Nigerians compared with ECG-LVH by SL voltage criteria alone or normal controls. CONCLUSION: The findings of this study support the fact that the ECG strain pattern is associated with increased LVM and an increased risk of developing abnormal LV geometry.

Diastole↗
PubMed1998

Comparison of irbesartan vs felodipine in the regression after 1 year of left ventricular hypertrophy in hypertensive patients (the SILVER trial). Study of Irbesartan in Left VEntricular hypertrophy Regression.

The SILVER (Study of Irbesartan in Left VEntricular hypertrophy Regression) trial is designed to test the hypothesis that the newly developed angiontensin-II receptor antagonist, irbesartan, will produce a greater reduction in left ventricular (LV) mass than felodipine ER, in a population of hypertensive patients defined by seated diastolic blood pressure (SeDBP) in the range 95-115 mmHg or seated systolic blood pressure (SeSBP) in the range 160-200 mm Hg. A population of 360 men and women of non-childbearing potential, >18 years of age, with hypertension, newly diagnosed or after a 3-week washout from previous anti-hypertensive or vasodilator therapies, will be randomised at approximately 80-90 European sites. Add-on therapy with hydrochlorothiazide and atenolol will be allowed for blood pressure control. Patients will be studied by two-dimensional and M-mode echocardiography at baseline (central validation of LV hypertrophy), on randomisation day, and after 6 and 12 months randomised therapy. Blinded analysis of echocardiograms will be performed at a central laboratory, which will provide measurements of the LV mass index (LVMI), determined by M-mode readings according to Devereux formula and using the Penn convention. The primary end-point of the study will be the change in LVMI from baseline to 12 months. The study power is 90% to detect differences between groups from baseline of approximately 8 g/m2.

Adolescent↗
PubMed1983

Relation of hemodynamic load to left ventricular hypertrophy and performance in hypertension.

Left ventricular hypertrophy and dysfunction in patients with hypertension are often poorly related to the level of blood pressure. To evaluate the reasons for this, 100 untreated patients (44 +/- 14 years) with essential hypertension were studied using cuff blood pressure and quantitative echocardiography to measure left ventricular mass index and end-diastolic relative wall thickness as 2 indexes of left ventricular hypertrophy. Left ventricular hypertrophy, as measured by either left ventricular mass index or end-diastolic relative wall thickness, correlated weakly with all indexes of blood pressure including systolic, diastolic, and mean blood pressure (r = 0.16 to 0.32). In contrast, end-diastolic relative wall thickness, an index which assesses the severity of concentric hypertrophy, showed a closer direct relation with total peripheral resistance (r = 0.52 p less than 0.001) and a significant inverse relation with cardiac index (r = -0.47, p less than 0.001). Left ventricular performance as assessed by fractional systolic shortening of left ventricular internal dimensions was not significantly related to left ventricular mass index, blood pressure, or peak systolic wall stress, but declined significantly with increasing mean systolic wall stress (r = -0.42, p less than 0.001) and even more with increasing end-systolic wall stress (r = -0.71, p less than 0.001). It is concluded that in patients with hypertension (1) left ventricular hypertrophy is correlated only modestly with measurements of resting blood pressure; and (2) the classic pattern of concentric left ventricular hypertrophy, as measured by relative wall thickness, is more closely related to the "typical" hypertensive abnormality of elevated peripheral resistance, suggesting that these anatomic and hemodynamic changes may be pathophysiologically interdependent. Furthermore, left ventricular performance declines when the pressure overload in hypertension is not offset by compensating hypertrophy, allowing wall stresses to increase.

Adolescent↗
PubMed1992

Limitations of the electrocardiographic diagnosis of left ventricular hypertrophy: the influence of left anterior hemiblock and right bundle branch block.

We analysed the performance of the electrocardiogram in diagnosing left ventricular hypertrophy in 70 patients with isolated left anterior hemiblock and in 75 patients with right bundle branch block, either isolated (44 cases) or associated (31 cases) with left anterior hemiblock. Left ventricular hypertrophy defined as an echocardiographically determined left ventricular mass greater than 261 g in men and 172 g in women or left ventricular mass index greater than 125 g/m2 in men and 112 g/m2 in women was present in 48 subjects (57%) with isolated left anterior hemiblock and 33 subjects (44%) with right bundle branch block. In patients with isolated left anterior hemiblock the best results were obtained using the SV1 or SV2 + (RV6 + SV6) greater than 25 mm with 74% in sensitivity and 67% in specificity; the criterion SIII + (R + S) maximal in a precordial lead greater than or equal to 30 mm showed a sensitivity of 74% but a specificity of 47%. In the whole group of patients with right bundle branch block none of the criteria nor combination of criteria achieved an acceptable performance (sensitivities ranged from 17% to 41% and specificities ranged from 54% to 85%). When these patients were divided according to the presence or absence of concomitant left anterior hemiblock the electrocardiographic indexes mostly showed, in comparison to whole group, higher values in sensitivity and lower values in specificity in right bundle branch block plus left anterior hemiblock and an opposite behaviour in isolated right bundle branch block.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Accelerated transmural gradients of energy compound metabolism resulting from left ventricular hypertrophy.

Eighteen dogs underwent transmural left ventricular biopsies for adenosine triphosphate and suturing of the noncoronary cusp, creating valvular aortic stenosis. Three months after aortic stenosis and the subsequent development of left ventricular hypertrophy, animals underwent repeat transmural left ventricular biopsies followed by total myocardial ischemia at 37 degrees C. Left ventricular tissue samples for adenosine triphosphate and lactate levels were determined at 15-minute intervals and compared with 15 control animals. No significant difference between subendocardial and subepicardial adenosine triphosphate levels was found between left ventricular samples taken before left ventricular hypertrophy and 3 months after left ventricular hypertrophy. Significant differences in adenosine triphosphate utilization occurred between subendocardial and subepicardial layers in control and left ventricular hypertrophy myocardium, however. The gradient between the subendocardium and the subepicardium was significantly increased by left ventricular hypertrophy (p less than 0.05). Significant differences also occurred within the same layer when left ventricular hypertrophy and control groups were compared. During total ischemia, lactate concentration was significantly greater within the subendocardium than within the subepicardium in left ventricular hypertrophy. The onset of ischemic contracture was 48.2 +/- 2.1 minutes in left ventricular hypertrophy versus 62.3 +/- 1.8 minutes in control hearts (p less than 0.01). Subendocardial intramyocardial pressure increased significantly earlier than subepicardial in both left ventricular hypertrophy and control hearts. Adenosine triphosphate was used, and lactate accumulated more rapidly in animals with a more pronounced hemodynamic gradient. These data show that after left ventricular hypertrophy, adenosine triphosphate stores in the subendocardium and the subepicardium are unchanged from control values, yet the rates of adenosine triphosphate utilization and lactate accumulation during total ischemia are significantly increased. Furthermore, the subendocardial to subepicardial gradient of adenosine triphosphate utilization during ischemia found in normal hearts is markedly increased by left ventricular hypertrophy.

Adenosine Triphosphate↗
PubMed1998

[Significance of left ventricular hypertrophy in hypertension].

Left ventricular hypertrophy (LVH) is supposed to be a useful marker of cardiovascular (CV) complications during the course of hypertension (HT). To evaluate it, authors compared the clinical findings in hypertensive patients (pts) with and without LVH defined by echocardiography (echo). Hospital records of hypertensives treated in the 1st Medical Department during the year 1995 were analysed. LVH was defined by echo (Penn convention) as left ventricular mass index (LVMI) > 125 g/m2 in men and > 115 g/m2 in women. Presence of LVH was found in 72 pts (mean age 66 y), absence of LVH in 38 pts (mean age 56 y). There were statistically significant more CV complications in LVH-positive pts (incidence of myocardial infarction, arrhythmias, heart failure, ischemia (ECG), mitral regurgitation) as in LVH-negative. Tendency for other complications in LVH-positive pts (incidence of renal failure, stroke, LV diastolic dysfunction and aortic regurgitation) was also present. LVH-positive pts were about ten years older than the LVH-negative. In other risk factors (LVH and age not included) the both groups of pts were matched. LVH in pts with HT brings usually a complicated course of the disease. Age is an important contributing factor. Authors recommend to look after LVH presence in hypertensives as it carries much more complicated course of the disease.

Adult↗
PubMed2006

Regression of left ventricular hypertrophy during antihypertensive treatment.

Left ventricular hypertrophy is a risk factor for cardiovascular events and stroke. It has been demonstrated that the regression of left ventricular hypertrophy (evaluated by 12-lead electrocardiography and by echocardiography) during antihypertensive treatment is associated with a lower risk of cardiovascular mortality and may thus improve the prognosis. Black people run a disproportionately high risk of developing essential arterial hypertension which frequently results in end organ damage, including left ventricular hypertrophy, haemorrhagic stroke and renal failure. We report a case of significant regression of left ventricular hypertrophy in a sub-Saharan African patient, during antihypertensive treatment.

Adult↗
PubMed1986

Reversal of left ventricular hypertrophy following treatment with beta-blockers: experience with tertatolol.

Hypertrophy in response to increasing blood pressure in primary hypertension leads to important functional consequences for the left ventricle. In fact, the progression of hypertensive heart disease, from an adaptive left ventricular hypertrophy with compensated ventricular function to severe hypertrophy with left ventricular failure, has been long thought to be related to the severity and duration of hypertension. Antihypertensive treatment seems to prevent or minimize the occurrence of left ventricular hypertrophy, but questions arise as to whether this therapy is also able to restore normal hemodynamic conditions, or at least to minimize the hemodynamic abnormalities. This review aims at summarizing current knowledge on the effects of the antihypertensive treatment with beta-blockers, including tertatolol, on hypertension-induced left ventricular hypertrophy. The pathogenetic mechanisms underlying the cardiovascular changes associated with hypertension are discussed. A decrease in left ventricular wall thickness as well as in left ventricular mass has been reported in most of the studies performed with different types of beta-adrenergic blocking agents. The extent of this reduction seems to be related not only to the fall in systemic blood pressure, but also to a decrease in sympathetic stimulation. With regard to the functional consequences of hypertension, the reversal of left ventricular hypertrophy following antihypertensive treatment with beta-blockers is usually associated with an improvement in left ventricular performance. This phenomenon can hardly be ascribed to the direct effects of beta-blocking agents. It is more likely to be related to the concomitant reduction in the afterload and to the improved left ventricular compliance, associated with a decrease in left ventricular wall thickness.

Adrenergic beta-Antagonists↗