Effects Of Left Ventricular Hypertrophy Research Articles

A propensity score-based case–control study of renin–angiotensin system gene polymorphisms and diastolic heart failure

Angiotensin II plays an important role in diastolic heart failure (DHF). However, genetic studies of DHF are scarce in the literature. We hypothesized that RAS genes might be the susceptible genes for DHF and conducted a propensity score-based case–control study to prove this hypothesis. A total of 666 subjects (285 diagnosed with DHF confirmed by echocardiography and 381 without diastolic dysfunction) were recruited. Genotyped were: the angiotensin-converting enzyme (ACE) gene insertion/deletion polymorphism; the T174M, M235T, G-6A, A-20C, G-152A and G-217A polymorphisms of the angiotensinogen (AGT) gene; and the A1166C polymorphisms of the angiotensin II type I receptor (AT1R) gene. Propensity scores (PS) were used to find patients with and without DHF with equalized characteristics. We also assembled another set of PS matched groups for all characteristics except left ventricular mass (LVM) to detect the genetic association with DHF through the effect of left ventricular hypertrophy. PS matched 210 patients with DHF to 210 without. In a single-locus analysis, the odds ratios (ORs) for DHF were significant with the ACE DD genotype (OR = 1.30, 95% CI = 1.13–1.49, permuted P = 0.003) and the AT1R 1166 CC genotype (OR = 2.61, 95% CI = 1.52–4.45, permuted P < 0.001). Significant gene–gene interaction between the two genes was also detected. However, the ACE gene effect was diminished if LVM was not controlled in the propensity scores. We concluded that genetic variants in the RAS genes may determine individual risk to develop DHF through different pathways. Concomitant presence of ACE DD and AT1R 1166 CC genotypes synergistically increased the predisposition to DHF.

Poster session V

Peak systolic strain rate (SR) has been proposed as a means for quantifying dobutamine stress echocardiography (DSE). However, myocardial deformation may be influenced by other processes including left ventricular hypertrophy (LVH). This study sought to investigate the effect of LVH on myocardial deformation at dobutamine stress echocardiography (DSE).

Distinct Cellular and Molecular Mechanisms Underlie Functional Remodeling of Repolarizing K + Currents With Left Ventricular Hypertrophy

Left ventricular hypertrophy (LVH) is associated with electric remodeling and increased arrhythmia risk, although the underlying mechanisms are poorly understood. In the experiments here, functional voltage-gated (Kv) and inwardly rectifying (Kir) K(+) channel remodeling was examined in a mouse model of pressure overload-induced LVH, produced by transverse aortic constriction (TAC). Action potential durations (APDs) at 90% repolarization in TAC LV myocytes and QT(c) intervals in TAC mice were prolonged. Mean whole-cell membrane capacitance (C(m)) was higher, and I(to,f), I(K,slow), I(ss), and I(K1) densities were lower in TAC, than in sham, LV myocytes. Although the primary determinant of the reduced current densities is the increase in C(m), I(K,slow) amplitudes were decreased and I(ss) amplitudes were increased in TAC LV cells. Further experiments revealed regional differences in the effects of LVH. Cellular hypertrophy and increased I(ss) amplitudes were more pronounced in TAC endocardial LV cells, whereas I(K,slow) amplitudes were selectively reduced in TAC epicardial LV cells. Consistent with the similarities in I(to,f) and I(K1) amplitudes, Kv4.2, Kv4.3, and KChIP2 (I(to,f)), as well as Kir2.1 and Kir2.2 (I(K1)), transcript and protein expression levels were similar in TAC and sham LV. Unexpectedly, expression of I(K,slow) channel subunits Kv1.5 and Kv2.1 was increased in TAC LV. Biochemical experiments also demonstrated that, although total protein was unaltered, cell surface expression of TASK1 was increased in TAC LV. Functional changes in repolarizing K(+) currents with LVH, therefore, result from distinct cellular (cardiomyocyte enlargement) and molecular (alterations in the numbers of functional channels) mechanisms.

Evidence of a Dominant Backward-Propagating “Suction” Wave Responsible for Diastolic Coronary Filling in Humans, Attenuated in Left Ventricular Hypertrophy

Coronary blood flow peaks in diastole when aortic blood pressure has fallen. Current models fail to completely explain this phenomenon. We present a new approach-using wave intensity analysis-to explain this phenomenon in normal subjects and to evaluate the effects of left ventricular hypertrophy (LVH). We measured simultaneous pressure and Doppler velocity with intracoronary wires in the left main stem, left anterior descending, and circumflex arteries of 20 subjects after a normal coronary arteriogram. Wave intensity analysis was used to identify and quantify individual pressure and velocity waves within the coronary artery circulation. A consistent pattern of 6 predominating waves was identified. Ninety-four percent of wave energy, accelerating blood forward along the coronary artery, came from 2 waves: first a pushing wave caused by left ventricular ejection-the dominant forward-traveling pushing wave; and later a suction wave caused by relief of myocardial microcirculatory compression-the dominant backward-traveling suction wave. The dominant backward-traveling suction wave (18.2+/-13.7 x 10(3) W m(-2)s(-1), 30%) was larger than the dominant forward-traveling pushing wave (14.3+/-17.6 x 10(3) W m(-2) s(-1), 22.3%, P =0.001) and was associated with a substantially larger increment in coronary blood flow velocity (0.51 versus 0.14 m/s, P <0.001). In LVH, the dominant backward-traveling suction wave percentage was significantly decreased (33.1% versus 26.9%, P =0.01) and inversely correlated with left ventricular septal wall thickness (r =-0.52, P <0.02). Six waves predominantly drive human coronary blood flow. Coronary flow peaks in diastole because of the dominance of a "suction" wave generated by myocardial microcirculatory decompression. This is significantly reduced in LVH.

The effects of left ventricular hypertrophy on the respiratory changes in transmitral Doppler flow patterns of hypertension patients

Left ventricular early diastolic fillings can be reduced by inspiration. However, the effects of left ventricular hypertrophy on such changes have not been studied before. This study was undertaken to investigate whether respiratory changes in transmitral Doppler flow were affected by left ventricular hypertrophy in hypertension patients. Eighty-three patients (mean age 46 +/- 8 years, 49 males) with untreated essential hypertension were included in this study. Transmitral Doppler flow velocity was measured both at end-expiration and end-inspiration. Left ventricular mass was measured by M-mode echocardiography. We divided patients into two groups based on the presence of left ventricular hypertrophy or not. Twenty-one patients were diagnosed to have left ventricular hypertrophy. In patients without left ventricular hypertrophy, the peak early filling velocity decreased significantly (from 74 +/- 15 to 71 +/- 18 cm s(-1), P = 0.003), the peak atrial velocity increased significantly (from 65 +/- 17 to 74 +/- 15 cm s(-1), P < 0.001) and the early filling to atrial velocity ratio decreased significantly (from 1.2 +/- 0.3 to 1.1 +/- 0.3, P < 0.001) from end-expiration to end-inspiration. In patients with left ventricular hypertrophy, the parameters of transmitral Doppler flow pattern did not change during respiration. Respiratory changes in the transmitral Doppler flow velocity are blunted by left ventricular hypertrophy in hypertension patients. This phenomenon is probably contributed by the increased left ventricular wall stiffness in the left ventricular hypertrophy.

Adverse effects of left ventricular hypertrophy in the reduction of endpoints in NIDDM with the angiotensin II antagonist losartan (RENAAL) study

We explored the impact of baseline left ventricular hypertrophy (LVH) and losartan treatment on renal and cardiovascular (CV) events in 1,513 patients from the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial, which studied the effects of losartan on the progression of renal disease and/or death in patients with type 2 diabetes and nephropathy. LVH was assessed using ECG criteria (Cornell product and/or Sokolow-Lyon voltage). The risk of renal or CV events was determined by a proportional hazards model fit with treatment allocation and presence of LVH. Covariates at baseline included age, sex, systolic BP, mean arterial pressure, pulse, proteinuria, serum creatinine, albumin and haemoglobin. A total of 187 subjects (12%) had LVH at baseline. Treatment with losartan resulted in a significant decrease in the Cornell product (-6.2%) and Sokolow-Lyon voltage (-6.3%). LVH was shown to be significantly associated with the primary endpoint, which was a composite of doubling of serum creatinine (DSCR), endstage renal disease (ESRD) or death (hazard ratio [HR]=1.44, p=0.011), as well as with the composite renal endpoint of DSCR/ESRD (HR=1.42, p=0.031) and CV events (HR=1.68, p=0.001). Losartan treatment of patients with LVH decreased the CV as well as renal risk to a level similar to that of patients without LVH. In patients with type 2 diabetes and nephropathy, LVH is associated with significantly increased risk of CV events and the progression of kidney disease. Importantly, in patients with LVH, losartan reduced the CV as well as the renal risk to a level similar to that seen in subjects without LVH.

Depolarization pattern of ventricular epicardium in two‐kidney one‐clip hypertensive rats

The present study is the first attempt to examine the effect of left ventricular hypertrophy (LVH) on the excitation pattern of the ventricular epicardium in experimental hypertensive rats. The left renal artery was clipped in Wistar rats (n = 8; 6-8 months old; weight, 174-295 g) to produce two-kidney one-clip (2K1C) hypertension. After 4 weeks, blood pressure was measured, and epicardial potential mapping was performed under sinus rhythm from 64 unipolar electrodes regularly distributed over the ventricular epicardium. Systolic blood pressure was approximately 40% higher in the rats with a clipped renal artery (162 +/- 14 mmHg, mean +/- s.d.) than in the normotensive rats (115 +/- 3 mmHg). LVH (approximately 23% increase in the ratio of the left ventricular weight to the body weight, P < 0.05) was observed in the 2K1C hypertensive rats. The depolarization pattern of the ventricular epicardium in the normotensive rats was similar to that in the rats with 2K1C hypertensive LVH. The duration of ventricular epicardial activation was shown to increase (approximately 35%, P < 0.05) in the hypertensive rats as compared to the normotensive animals. This study provides an explanation for alterations of the body surface potential distribution in hypertensive patients with LVH.

W17-P-007 Effects of left ventricular hypertrophy on transmitral flow pattern and aortic stiffness

W17-P-007 Effects of left ventricular hypertrophy on transmitral flow pattern and aortic stiffness

Comparison of the prognostic value of left ventricular hypertrophy in African-American men versus women

Echocardiographically determined left ventricular (LV) hypertrophy may be a stronger risk factor of cardiovascular disease (CVD) for women than for men, although it is unclear whether reported gender differences are real or attributable to confounding. We evaluated echocardiographic LV hypertrophy (defined as LV mass/height(2.7) >/=51 g/m(2.7)) collected from the African-American population of the Atherosclerosis Risk in Communities Study. Incident CVD events (57 in men, 62 in women) were determined during a median follow-up of 4.9 years (interquartile range 4.3 to 5.6) and included nonfatal myocardial infarction, cardiac death, coronary revascularization, and stroke. We conducted 2 analyses. First, we created matched samples of 340 men and 812 women who had LV hypertrophy based on propensity score and estimated the gender-specific incidence rate ratios and population-attributable risks. Second, we evaluated the complete cohort (604 men and 1,113 women) with Poisson's regression after adjusting for age, body mass index, hypertension, diabetes mellitus, ratio of total cholesterol to high-density lipoprotein cholesterol, current smoking, and education level. LV hypertrophy was significantly predictive of incident CVD, and the association shown by analyses of matched propensity scores was similar in men and women (incidence rate ratio 1.88 vs 1.92, p = 0.97 for men, population-attributable risk 0.22 vs 0.26, p <0.07 for women). In the multivariate analysis, we found comparable effect estimates for LV hypertrophy (incidence rate ratio 1.66 vs 2.09, p = 0.55 for men; population-attributable risk 0.24 vs 0.32, p <0.07 for women). Thus, LV hypertrophy is a strong predictor of CVD in African-Americans, and the effect of LV hypertrophy on CVD is similar in men and women.

Angiotensin-converting enzyme I/D gene polymorphisms and effects of left ventricular hypertrophy in Turkish myocardial infarction patients

Objective — Since the initial report of the association of the deletion/insertion (D/I) polymorphism in the gene for angiotensin-converting enzyme (ACE) with myocardial infarction (MI), there has been considerable controversy. Some have found the D allele to be associated with MI, coronary heart disease (CHD) or other cardiac pathologies, while others have not. In view of the clinical importance of the ACE as a major marker of cardiovascular diseases, we investigated the I/D polymorphism of the ACE gene in Turkish patients with acute myocardial infarction in comparison with control subjects.Methods and results — Polymerase chain reaction, and agarose gel electrophoresis techniques were used to determine the ACE genotype in 214 subjects. The frequencies of ACE D and ACE I allele among the patiens with acute myocardial infarction were 65.54% and 36.45% and in the control subjects 57.62% and 42.37%, respectively. ACE DD genotypes were found higher in patients with left ventricular hypertrophy (LVH) than without LVH (55.6% vs. 37.7%; X2: 2.534, p > 0.05).Conclusions — The ACE D allele is more frequent in patients with acute myocardial infarction than in controls. Moreover ACE DD genotype might be associated with an increased risk of left ventricular hypertrophy.

QT dispersion in patients with different etiologies of left ventricular hypertrophy: the significance of QT dispersion in endurance athletes

Left ventricular hypertrophy (LVH) increases the risk of ventricular arrhythmias and sudden death and has a significant effect on total cardiovascular mortality. QT dispersion (QTd) is a measure of inhomogeneous repolarization and is used as an indicator of arrhythmogenicity. In this study we detected QTd in patients with different etiologies of left ventricular hypertrophy and the effect of LVH in QTd on endurance athletes. The study group consisted of 147 white male subjects with 3 different etiologies of LVH and 30 healthy male individuals. The underlying etiologies of LVH were essential hypertension, valvular aortic stenosis and long-term training (athletic heart). QTd was measured by surface electrocardiogram and Bazett’s formula was used to correct QTd for heart rate (QTcd). Left ventricular mass was determined by transthoracic echocardiography and left ventricular mass index was calculated in relation to body surface area. The QTcd was significantly higher in patients with pathological LVH (due to hypertension and aortic stenosis) than in the athletes’ group (physiological LVH) and healthy subjects ( P<0.05). The magnitude of QTcd was similar between athletes and the control group ( P=0.6). The difference of QTcd between the groups with pathological LVH was not statistically significant ( P=0.1). In conclusion; the increasing of QT dispersion is associated with only pathological conditions of LVH. The left ventricular hypertrophy has not a negative effect in QT dispersion on endurance athletes. The measurement of QT dispersion may be a non-invasive useful method for screening additional pathological conditions in endurance athletes.

Ventricular hypertrophy amplifies transmural repolarization dispersion and induces early afterdepolarization.

The effects of left ventricular hypertrophy (LVH) on the generation of phase 2 early afterdepolarization (EAD) and transmural dispersion of repolarization (TDR) were assessed using arterially perfused rabbit ventricular wedge preparations. Transmembrane action potentials from epicardium, subendocardium, and endocardium were simultaneously recorded together with a transmural ECG. Transmural action potential duration (APD) was also mapped. LVH (renovascular hypertension model) produced significant prolongation in ventricular APD and QT interval. Preferential APD prolongation in subendocardium and endocardium was associated with a marked increase in TDR. Phase 2 EADs were generated from subendocardium or endocardium in all LVH rabbits (15 of 15) in the absence of APD prolonging agents at basic cycle lengths of 2,000-4,000 ms. Phase 2 EAD could produce "R on T" extrasystoles, initiating polymorphic ventricular tachycardia (VT). This study provides the first direct evidence from intracellular recordings that phase 2 EAD could be generated from rabbit intact hypertrophied LV wall in the absence of APD prolonging agents, resulting in R on T extrasystoles capable of initiating polymorphic VT under enhanced TDR.

Left ventricular hypertrophy decreases slowly but not rapidly activating delayed rectifier potassium currents of epicardial and endocardial myocytes in rabbits.

Delayed rectifier K(+) currents are critical to action potential (AP) repolarization. The present study examines the effects of left ventricular hypertrophy (LVH) on delayed rectifier K(+) currents and their contribution to AP repolarization in both epicardial (Epi) and endocardial (Endo) myocytes. VH was induced in rabbits by a 1-kidney removal, 1-kidney vascular clamping method. Slowly (I(Ks)) and rapidly (I(Kr)) activating delayed rectifier K(+) currents were recorded by the whole-cell patch-clamp technique, and APs were recorded by the microelectrode technique. In normal rabbit left ventricular myocytes, I(Ks) densities were larger in Epi than in Endo (1.1+/-0.1 versus 0.43+/-0.07 pA/pF), whereas I(Kr) density was similar between Epi and Endo (0.31+/-0.05 versus 0.36+/-0.07 pA/pF) at 20 mV. LVH reduced I(Ks) density to a similar extent (approximately 40%) in both Epi and Endo but had no significant effect on I(Kr) in either Epi or Endo. Consequently, I(Kr) was expected to contribute more to AP repolarization in LVH than in control. This was confirmed by specific I(Kr) block with dofetilide, which prolonged AP significantly more in LVH than in control (31+/-3% versus 18+/-2% in Epi; 53+/-6% versus 32+/-4% in Endo at 2 Hz). In contrast, L-768,673 (a specific I(Ks) blocker) prolonged AP less in LVH than in control. The very small I(Ks) density in Endo with LVH is consistent with the greater incidence of early afterdepolarizations induced in this region by dofetilide. LVH induces a decrease in I(Ks) density and increases the propensity to develop early afterdepolarizations, especially in Endo.

Protective effect of left ventricular hypertrophy in right coronary artery occlusions.

To test the hypothesis that left ventricular hypertrophy (LVH) reduces the electrocardiographic and functional effects of right coronary artery occlusion. We analysed 215 patients (166 males and 49 women, age of 58.9 +/- 10.6 years), with occlusion of the right coronary artery without other associated lesions. There was no significant difference (p > 0.05) in age and gender distribution between the 78 patients with LVH (left ventricular mass > 100 g/m2) (Group A) when compared with the 137 patients without LVH (left ventricular mass < 100 g/m2) (Group B). The electrocardiographic finding of transmural necrosis was more often found in group B patients than in group A patients (56.9% and 30.8%, respectively; p < 0.05). The left ventricular function parameters of group A were better than those of group B: the ratio end-diastolic pressure/systolic pressure (EDP/SP) (A: 0.108 +/- 0.036; B: 0.121 +/- 0.050; p < 0.05); the end-diastolic volume index (A: 75.9 +/- 31.3 ml/m2; B: 88.0 +/- 31.0 ml/m2; p < 0.01); the end-systolic volume index (A: 16.0 +/- 10.0 ml/m2; B: 27.0 +/- 20.0 ml/m2; p < 0.001); the ejection fraction (A 78.6 +/- 10.8%; B 67.7 +/- 17.9%; p < 0.001); the anteroinferior shortening (A: 43.9 +/- 10.3%; B: 35.1 +/- 12.8%; p < 0.001). A higher degree of coronary tortuosity was observed in group A than in group B (78.2% and 24.1%; p < 0.001) and also a more frequent absent or minimal diaphragmatic hypokinetic area (A: 80.8%; B: 54.0%; p < 0.05). LVH reduces the effects of myocardial sequela and protects LV function when right coronary occlusion develops.

Effects of left ventricular hypertrophy on force and Ca2+ handling in isolated rat myocardium.

To study the effect of left ventricular (LV) hypertrophy on force and Ca2+ handling in isolated rat myocardium, LV hypertrophy was induced in rats by banding of the abdominal aorta. After 16 wk, arterial pressure was assessed by catheterization. LV trabeculae were isolated and loaded with indo 1 salt by iontophoretic injection. Isometric force and intracellular free Ca2+ concentration ([Ca2+]i) were measured at stimulation frequencies between 0.25 and 3 Hz and rest intervals between 2 and 240 s. Sarcoplasmic reticulum (SR) Ca2+ content was also investigated using rapid cooling contractures (RCC). Systolic and diastolic pressure as well as heart weight-to-body weight ratios were significantly elevated in banded compared with control animals (167 vs. 117 mmHg, 108 vs. 83 mmHg, and 4.6 vs. 4.0 mg/g, respectively). At high frequencies, twitch relaxation and [Ca2+]i decline rates were significantly slower in banded compared with control rats, and diastolic [Ca2+]i was higher in the banded rat muscles (at 3 Hz, force half-time = 83 vs. 68 ms; time constant of [Ca2+]i decline = 208 vs. 118 ms; and diastolic [Ca2+]i = 505 vs. 353 nM). These differences could not be ascribed to altered Na+/Ca2+ exchange, since twitch relaxation and Ca2+ handling were not different between groups in the presence of caffeine (or cyclopiazonic acid plus ryanodine), where relaxation depends primarily on Na+/Ca2+ exchange. After long rest intervals (> or = 120 s), control rats showed a significant rest potentiation of force and Ca2+ transients, whereas banded rats did not. In addition, RCC amplitudes increased with rest in control but were unaltered in banded rats. In summary, pressure-overload hypertrophy was associated with slower twitch relaxation and [Ca2+]i decline but also with blunted rest potentiation of twitches and SR Ca2+ content of LV trabeculae. The decrease in SR Ca(2+)-ATPase function in banded rats may contribute to the observed diastolic dysfunction associated with pressure-overload hypertrophy.

Aging and Essential Hypertension: Effect of Left Ventricular Hypertrophy on Cardiac Function

This study was designed to analyze the cardiac effects of aging and of hypertension in patients with essential hypertension and with or without left ventricular hypertrophy (LVH). Thirty-one patients <55 years old and 66 patients >64 years old with essential hypertension were divided according to the presence or absence of LVH. Cardiac functional structure was assessed by 2D-guided M-mode echocardiography. The peak filling rate and the duration of rapid filling were obtained by digitizing septal and posterior wall echoes. In the older group only was systolic function significantly impaired in subjects with LVH when compared with subjects without LVH [velocity of circumferential fiber shortening (L/msec): 1.40 ± 0.24 v 1.18 ± 0.25; fractional fiber shortening (%): 43.06 ± 5.02 v 36.26 ± 7.1; ejection fraction (%): 81.1 ± 5.1 v 73.13 ± 9.2; P < .05]. Older patients, even without LVH, showed a longer duration of rapid filling (321.0 ± 108.3 msec) and lower peak filling rate (7.01 ± 1.86 cm/sec) in comparison with younger persons with or without LVH. In the older subjects the increase in left ventricular mass was associated with a decrease of velocity of circumferential fiber shortening (r = −0.48, P < .01), fractional fiber shortening (r = −0.40, P < .01), and ejection fraction = −0.50, P < .01), whereas there was no correlation in the younger group. The present findings of impaired diastolic filling even in the absence of LVH in the elderly, and the deterioration of systolic function parallel to the increase in LV mass suggest that aging is associated with a decrease in the number of functioning contractile elements per unit of cardiac mass.

Significance of QTc prolongation on ventricular arrhythmias in patients with left ventricular hypertrophy secondary to essential hypertension

The present study was designed to detect the arrhythmogenic effect of left ventricular hypertrophy, QTc prolongation and the relationship between the QTc duration and ventricular arrhythmias in patients with left ventricular hypertrophy secondary to essential hypertension. Sixty-eight hypertensive patients (51 male and 17 female, mean age 52±6 years) and 30 healthy normotensive subjects (22 male and eight female, mean age 49±6 years) were enrolled in the study. The frequency of ventricular arrhythmias was investigated with 24-h ambulatory electrocardiographic monitoring and grade 3 and 4 ventricular arrhythmias according to a modified Lown and Wolf classification were accepted as complex arrhythmias. The echocardiographic features of the patients were divided into five groups as follows: (1) normal left ventricular diameter and wall thickness, (2) concentric left ventricular hypertrophy, (3) asymmetric septal hypertrophy, (4) dilated left ventricle, (5) dilated and hypertrophic left ventricle. The frequency of complex ventricular ectopia and the QTc duration were estimated for each group and compared with Student's t-test. Left ventricular hypertrophy was detected in 38 of 68 patients (56%) with essential hypertension. In patients with left ventricular hypertrophy, the incidence of complex ventricular arrhythmias was two- and fivefold higher compared with patients without left ventricular hypertrophy and with controls, respectively. All of the patients with echocardiographic left ventricular dilatation had experienced complex ventricular arrhythmias. QTc duration correlated positively with left ventricular mass index and left ventricular internal diastolic dimension. The highest QTc intervals were detected in patients with left ventricular hypertrophy and complex arrhythmias. In patients with left ventricular hypertrophy, a QTc duration longer than 380 ms had a sensitivity of 74% and a specificity of 89% for detecting complex ventricular arrhythmias. It is concluded that patients with left ventricular hypertrophy have a higher incidence of complex ventricular arrhythmias and QTc prolongation in those patients can be a good marker for the increased risk of arrhythmias.

Homogeneously Reduced Versus Regionally Impaired Myocardial Blood Flow in Hypertensive Patients: Two Different Patterns of Myocardial Perfusion Associated With Degree of Hypertrophy

Objectives. The aim of this study was to quantitatively measure regional and global myocardial blood flow and coronary reserve in hypertensive patients without coronary artery disease and to assess the correlation with left ventricular mass.Background. The effect of left ventricular hypertrophy on regional vasodilating coronary capability in arterial hypertension is controversial, and no quantitative method has been applied to assess a possible correlation.Methods. Positron emission tomography was performed in 50 untreated hypertensive patients and 13 normotensive subjects. Blood flow at baseline and after dipyridamole was globally and regionally measured by using nitrogen-13 ammonia; coronary reserve and resistance were calculated. Left ventricular mass was assessed by two-dimensional echocardiography.Results. In hypertensive patients, flow at baseline was similar to that of normotensive subjects (p = 0.21), but values were reduced after pharmacologic vasodilation (p < 0.05). This impairment of maximal coronary flow was not correlated with left ventricular mass (p = 0.13). Among hypertensive patients, we identified a group with a homogeneous distribution of perfusion and a group with a heterogeneous flow pattern. Flow was globally reduced in the former group, but it was abnormal only at the site of perfusion defects in the latter. Patients with regional defects showed the highest likelihood of having an increased left ventricular mass.Conclusions. In arterial hypertension, left ventricular mass is not correlated with global myocardial blood flow. Nevertheless, patients with ventricular hypertrophy are likely to show a heterogeneous flow pattern with regional defects and almost normal blood flow in nonaffected regions. In hypertensive patients with a homogeneous perfusion pattern during stress, myocardial blood flow frequently shows a diffuse reduction.

C8 Effects of left ventricular hypertrophy on myocardial blood flow, oxygen consumption and glucose uptake in essential hypertension

C8 Effects of left ventricular hypertrophy on myocardial blood flow, oxygen consumption and glucose uptake in essential hypertension

Heart rate variability in left ventricular hypertrophy

BACKGROUND--Electrocardiographic left ventricular hypertrophy and strain are associated with increased cardiac morbidity and mortality. Impaired cardiac autonomic function, assessed non-invasively by spontaneous heart rate variability on Holter monitoring, is associated with an increased risk of sudden death after myocardial infarction. AIM--To study the effect of left ventricular hypertrophy on heart rate variability. PATIENTS--36 controls and 154 patients with left ventricular hypertrophy (94 with hypertension and 60 with aortic valve disease). SETTING--Tertiary referral centre. METHODS--Heart rate variability was measured on 24 h Holter recordings by non-spectral methods. Left ventricular mass index and fractional shortening were measured by echocardiography. RESULTS--Patients with left ventricular hypertrophy had a higher left ventricular mass index (P < 0.001) and reduced heart rate variability (P < 0.001) compared with those of the controls. A continuous inverse relation was apparent between heart rate variability and left ventricular mass index (r = -0.478, P < 0.001). Heart rate variability was not affected by age, the presence of coronary artery disease in patients with left ventricular hypertrophy, or beta blocker treatment for hypertension. Multivariate analysis showed that left ventricular mass index is the most important determinant of heart rate variability. CONCLUSION--Heart rate variability is significantly reduced in patients with left ventricular hypertrophy secondary to hypertension or aortic valve disease. A continuous inverse relation exists between heart rate variability and left ventricular mass index. Impaired cardiac autonomic function in left ventricular hypertrophy may contribute to the mechanism of sudden death.