Regression of hypertensive heart hypertrophy caused by chronic angiotensin-converting enzyme inhibition

We wanted to determine whether an antihypertensive therapy with the angiotensin-converting enzyme inhibitor enalapril can induce regression of hypertensive hypertrophy. 13 patients with hypertensive left ventricular hypertrophy were treated with enalapril (10-40 mg/day) for 9 months. Left ventricular pump function, left ventricular hypertrophy and geometry were studied by echocardiography before and 3, 6 and 9 months after enalapril treatment had been established. Both a decrease in systolic arterial blood pressure as well as a reversal of myocardial hypertrophy was obtained. After 3 months' therapy, systolic arterial blood pressure dropped from 189 +/- 8 to 171 +/- 9 mm Hg and left ventricular muscle mass decreased from 210 +/- 13 to 196 +/- 8 g/m2. After 6 months' therapy, systolic arterial blood pressure decreased further to 154 +/- 7 mm Hg and left ventricular muscle mass to 181 +/- 8 g/m2. After another 3 months' therapy (after 9 months) no further decrease in systolic arterial blood pressure (159 +/- 9 mm Hg), and no further decrease in left ventricular muscle mass (189 +/- 8 g/m2) were obtained. After 9 months' therapy, reversal of myocardial hypertrophy was adequate in relation to the amount of blood pressure lowering. Due to unaltered ventricular loading conditions, as evidenced by identical systolic wall stress values, left ventricular pump function remained unchanged.     

Relation between left ventricular midwall function and coronary vasodilator capacity in arterial hypertension

In systemic hypertension, depressed left ventricular midwall shortening predicts an adverse outcome and is associated with increased left ventricular relative wall thickness, which has been proposed as an independent predictor of cardiovascular risk and reduced coronary reserve. This study was designed to investigate whether depressed midwall shortening is associated with more critical impairment of coronary function and with exercise-induced myocardial ischemia. Sixty untreated hypertensive patients without coronary artery stenosis and 20 normotensive volunteers underwent exercise ECG testing, standard and transesophageal echocardiography to assess the occurrence of exercise-induced myocardial ischemia, left ventricular mass, geometry, and midwall shortening, and coronary vasodilator capacity. Compared with hypertensive patients with normal midwall shortening, those with depressed function (n=15) had higher minimum coronary resistance (1.19+/-0.27 versus 1.39+/-0.20 mm Hg/cm per second, P<0.01) and prevalence of exercise-induced myocardial ischemia (36 versus 67%, P<0.05). Within the hypertensive group, midwall shortening was inversely related to minimum coronary resistance (r=-0.42, P<0.01). Compared with patients with an exercise ECG test negative for myocardial ischemia, those with a positive test result (n=26) had higher minimum coronary resistance (1.13+/-0.21 versus 1.38+/-0.27 mm Hg/cm per second, P<0.01) and lower midwall shortening (104+/-16 versus 93+/-14%, P<0.01). We conclude that hypertensive patients with depressed midwall shortening have more severe impairment of coronary function and a higher prevalence of exercise-induced myocardial ischemia as compared with hypertensive patients with normal midwall shortening. These findings suggest that a decrease in myocardial performance may be related, at least in part, to chronic intermittent myocardial ischemia caused by a critical impairment of coronary vasodilator capacity.     

Regression of hypertrophy following nitrendipine: effect on systolic and diastolic function

The purpose of the present study was to determine whether an antihypertensive treatment with the dihydropyridine nitrendipine can induce regression of severe hypertensive hypertrophy and, whether alterations in systolic and diastolic ventricular function do occur. Eleven patients (age 49 +/- 11 years) with hypertensive hypertrophy were treated with nitrendipine (10-40 mg/day) for 12 months. Before and after therapy left ventricular hypertrophy, systolic, and diastolic function were measured by M-mode, two-dimensional- and digitized M-mode echocardiography. Systolic blood pressure dropped from 185.5 +/- 19.8 to 164.1 +/- 15.6 mm Hg (p less than 0.05). Left ventricular muscle mass was reduced from 234.5 +/- 51.2 to 201.5 +/- 37.9 g/m2 (p less than 0.05). Systolic wall stress (257.2 +/- 50.5 vs 245.2 +/- 44.4 x 10(3) dyn/cm2) and fractional shortening (34.9 +/- 6.1 vs 37.1 +/- 5.4%) remained nearly unchanged. The peak rate of left ventricular internal dimension change during diastole (MLVD), as an index of rapid early diastolic filling was increased (13.1 +/- 3.0 vs 16.5 +/- 3.7 cm/s; p less than 0.01), the relaxation time index, as an index of isovolumic relaxation, remained nearly unchanged (76 +/- 35 vs 64 +/- 24 ms; n.s.). A long-term treatment with nitrendipine regressed hypertensive left ventricular hypertrophy in proportion to blood pressure reduction. While systolic function remained unchanged as a consequence of an unaltered systolic wall stress, i.e. afterload, diastolic filling was markedly improved due to changes in left ventricular geometry through reduction in mass to volume ratio. Since relaxation time index remained nearly unchanged, factors contributing to the phase of isovolumic relaxation were not essentially affected by regression of left ventricular hypertrophy.     

Echocardiographic follow-up of patients with Takayasu's arteritis: five-year survival

Takayasu's arteritis (TA) is a primary vasculitis that causes stenosis or occlusion, rarely aneurysm and distal ischemia. This study was undertaken to examine cardiovascular damage using echocardiography and determine the causes of morbid-mortality in Mexican Mestizo patients with TA. Seventy-six patients were studied by transthoracic echocardiography. Left ventricular diameters, parietal thickness, systolic function, and wall motion were analyzed, also, valvular lesions and aorta features were assessed. Thickness of the interventricular septum was 12 mm +/- 3 (8-19), and that of posterior wall was 12 mm +/- 2 (9-18). The average left ventricular diastolic diameter was 47 mm +/- 7 (33-68) and the left ventricular systolic diameter 32 mm +/- 8 (16-64). The left ventricular ejection fraction was of 57 +/- 11%. Left ventricular concentric hypertrophy was found in 28 (50%) of the 56 hypertensive patients. The five-year survival of patients with left ventricular concentric hypertrophy was 80%, compared to 95% in patients without hypertrophy (P = 0.00). Abnormal wall motion was found in 15 patients. Thirty-one patients had aortic regurgitation, 19 had mitral regurgitation, 13 had tricuspid regurgitation, and 10 and pulmonary hypertension. Six patients had aneurysms of ascending aorta and 7 stenosis of descending aorta. Thirteen of 76 patients died (17%), 85% were hypertensive, and 9% also had acute myocardial infarction (AMI). Echocardiography, a noninvasive technique, shows a great utility in detection and follow-up of cardiovascular manifestations in patients with TA. New techniques, more sensitive toward detecting the early stages of left ventricular dysfunction, are promising to limit left ventricular hypertrophy development.     

Coronary vasodilator capacity and exercise-induced myocardial ischemia are related to the pulsatile component of blood pressure in patients with essential hypertension

OBJECTIVES: High pulsatile load is associated with structural alterations of the heart and arteries, which may cause changes in the coronary circulation and predispose to myocardial ischemia. This study was designed to investigate the relationships of coronary vasodilator capacity and exercise-induced myocardial ischemia to pulsatile and steady components of office blood pressure. METHODS: Eighty-two untreated, middle-aged hypertensive patients without coronary artery stenosis and 23 normotensive volunteers, underwent exercise electrocardiogram test and standard and transesophageal echocardiography to assess the occurrence of myocardial ischemia, left ventricular (LV) mass and geometry, total arterial compliance and coronary vasodilator capacity. RESULTS: In the hypertensive population, minimum coronary resistance (MCR) was significantly higher (P < 0.01) in the top as compared to all three lower pulse pressure (PP) quartiles (1.10 +/- 0.19, 1.21 +/- 0.23, 1.20 +/- 0.26 and 1.43 +/- 0.26 mmHg s/cm). An additional increase in MCR also occurred in the top quartile of systolic blood pressure (SBP), but not across quartiles of mean blood pressure. In regression analysis, MCR increased with PP, SBP and LV wall thickness and decreased with total arterial compliance. As compared to hypertensive patients with a negative exercise test for myocardial ischemia (n = 30), those with a positive test (n = 20) had higher MCR (1.12 +/- 0.22 versus 1.39 +/- 0.29 mmHg s/cm, P < 0.01) and lower total arterial compliance (96 +/- 22 versus 81 +/- 16%, P < 0.01). CONCLUSIONS: In untreated middle-aged hypertensive patients, coronary vasodilator capacity declines with increasing office PP and SBP. A decreased arterial compliance and increased LV wall thickness appear to be major alterations underlying this relationship. Exercise-induced myocardial ischemia is associated with higher MCR and lower arterial compliance.     

Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion

Prolonged nontransmural ischemia was produced and the early and late effects of reperfusion were studied in 10 conscious dogs instrumented over the long term. Five hours of partial circumflex coronary artery stenosis was produced with a hydraulic occluder, followed by gradual release over 20 min, with measurements of left ventricular pressure, regional myocardial function (systolic wall thickening by sonomicrometry), coronary blood flow velocity (pulsed Doppler), and myocardial blood flow (microspheres). During coronary stenosis the occluder was adjusted frequently to maintain a reduction of systolic wall thickening to 50% to 75% of control (average 62.6% of control). Myocardial blood flow in the ischemic area at 4 hr of partial coronary stenosis was reduced in the inner layers of the myocardium (subendocardium, from 0.81 +/- 0.18 at control to 0.36 +/- 0.08 SD, p less than .01; midwall, from 0.77 +/- 0.20 to 0.46 +/- 0.07 ml/min/g, p less than .01), accompanied by significant ST segment elevation on the subendocardial electrogram (0.83 +/- 0.96 to 4.58 +/- 4.10 mV; p less than .05) and decreased left ventricular dP/dt (3503 +/- 462 to 2991 +/- 339 mm Hg/sec; p less than .01). Within a few minutes after complete release of partial coronary stenosis, ST segments returned to control and myocardial blood flow of the inner layers was increased (subendocardium, 1.37 +/- 0.39, p less than .01; midwall, 0.97 +/- 0.28, p less than .05), but systolic wall thickening and left ventricular dP/dt were significantly depressed and remained reduced at 24, 48, and 72 hr when myocardial blood flow was normal. By seven days, systolic wall thickening and left ventricular dP/dt had returned to control (94.1 +/- 7.0% of control, 3353 +/- 605 mm Hg/sec, respectively; NS). Histologic changes caused by ischemia constituted only 2.7% (average) of the tissue between the crystals in the ischemic wall, but ischemic damage in the posterior papillary muscle, which did not contain crystals, was 31.9%. Thus, regional myocardial dysfunction reduced by nontransmural ischemia for 5 hr persisted for at least 3 days, with only slight damage to the left ventricular free wall but considerable infarction of the posterior papillary muscle. Full recovery of regional and global contractile function of the free wall then occurred within a period of 1 week.     

Myocardial perfusion in hypertensive patients with normal coronary angiograms

BACKGROUND: Pressure-induced left ventricular hypertrophy is one of the mechanisms responsible for an impaired coronary vasodilating capacity leading to myocardial ischemia and angina.The aim of the study was to investigate myocardial perfusion using cardiovascular magnetic resonance in patients with arterial hypertension and a history of chest pain and normal coronary angiography, and to estimate the influence of left ventricular hypertrophy on the parameters of myocardial perfusion. METHODS: The study included 102 patients (mean age 55.4 +/- 7.7 years) with well controlled hypertension and 12 healthy volunteers. In 96 patients, myocardial first-pass perfusion cardiovascular magnetic resonance both at rest and during an infusion of adenosine 140 microg/kg/min was performed. Semiquantitative perfusion analysis was performed by using the upslope of myocardial signal enhancement to derive the myocardial perfusion index and the myocardial perfusion reserve index. The study group was divided according to the presence of left ventricular hypertrophy in the cardiovascular magnetic resonance examination: group with left ventricular hypertrophy (n = 40) and without left ventricular hypertrophy (n = 56). RESULTS: Independent of the presence of left ventricular hypertrophy, there were significant differences in baseline myocardial perfusion index between hypertensive patients and controls (0.13 +/- 0.07 vs. 0.04 +/- 0.01; P < 0.001), and in stress myocardial perfusion index (hypertensive patients 0.21 +/- 0.10 vs. controls 0.09 +/- 0.03; P < 0.001). In hypertensive patients, the myocardial perfusion reserve index was reduced in the mid and apical portions of the left ventricle (1.71 +/- 1.1 vs. 2.52 +/- 0.83; P < 0.02). There was no significant correlation of myocardial perfusion reserve index with left ventricular mass or hypertrophy. CONCLUSION: In patients with mild or moderate hypertension and a history of chest pain with normal coronary angiography, there is regional myocardial perfusion reserve impairment that is independent of the presence of left ventricular hypertrophy and may be a reason for angina.     

Assessment of regional myocardial systolic function in hypertensive left ventricular hypertrophy using harmonic myocardial strain imaging

OBJECTIVES: Regional myocardial systolic function in hypertensive left ventricular hypertrophy was assessed using the newly developed myocardial strain imaging. METHODS: This study included 17 patients with hypertensive left ventricular hypertrophy (LVH group) and 22 normal subjects (N group). The transmural location of the strain peak value (StPP), and the strain peak value (StPV) in the end-systolic phase were measured at the posterior wall by myocardial strain imaging. Left ventricular mass index was simultaneously measured in both groups. RESULTS: StPV was significantly lower in the LVH group than the N group (1.00 +/- 0.36 vs 1.38 +/- 0.42, p < 0.01) and StPP was significantly moved to the epicardium side compared with the N group (31 +/- 10% vs 11 +/- 5%, p < 0.0001). StPV decreased and StPP increased with greater left ventricular mass index (r = -0.61, p < 0.0001; r = 0.72, p < 0.0001, respectively). CONCLUSIONS: Myocardial systolic impairment in hypertensive left ventricular hypertrophy may occur from the endocardium side, and the impairment may progress with increased left ventricular hypertrophy.     

Silent ST depression and cardiovascular end-organ damage in newly found, older hypertensives

In hypertension, both reduced vascular supply and increased cardiac demand contribute to the development of (silent) myocardial ischemia. Our aim was to determine the prevalence of ST-segment depression and to analyze contributing factors in asymptomatic, previously untreated, older hypertensives. From a population survey, in 184 patients with mild hypertension (4 times systolic blood pressure >/=160 mm Hg and/or diastolic blood pressure >/=95 mm Hg), 60 to 75 years of age, cardiovascular end-organ damage was measured. Episodes of ST-segment depression were measured by 48-hour ambulatory Holter monitoring and were observed in 21 hypertensives (12%). They showed a significantly higher combined far-wall intima-media thickness of carotid and femoral arteries and more arterial plaques as measured by B-mode ultrasound compared with hypertensives without ST depression (0.00098+/-0.00021 versus 0.00088+/-0.00016 mm and 5.2+/-3.7 versus 3.7+/-2.8 plaques, P<0.05, respectively), whereas left ventricular mass index was not different (111+/-18 versus 104+/-24 g/m(2); P=0.18, respectively). In hypertensives with transient ST-segment depression, a significant relation was found between left ventricular mass and ischemic burden (r=0.51, P=0.02). Approximately 1 of 8 unselected and previously untreated older hypertensives show asymptomatic ST-segment depression, suggestive of silent myocardial ischemia. These data suggest that vascular factors mainly determine the occurrence of ischemic ST-segment depression and cardiac factors determine the ischemic burden in older hypertensives.     

老年高血压左室肥厚患者的室性心律失常与心肌缺血

目的　了解老年原发性高血压左室肥厚患者的室性心律失常、心肌缺血的特点及两者的关系。方法　 90例老年 (≥ 6 0岁 )高血压患者经超声心动图测定左室质量指数 (LVMI) ,分为左室肥厚 (A组 )和非左室肥厚 (B组 )。经2 4h动态心电图测定 2 4h室性早搏总数 (VPCs)、Lown’s分级、ST段压低程度、持续时间及 2 4h发作次数。结果　A组室性心律失常的发生率明显增加 (P <0 .0 5 ) ,室性早搏 :75 %比 5 4% ,Lown’s 3～ 4级 :2 6 %比 4%。A组发作性ST段压低的发生率高 ,缺血持续时间长 (5 0 %比 15 % ,P <0 .0 5 )。所有缺血发作均为无症状性。室性心律失常与心肌缺血的昼夜节律变化基本相同。结论　无冠心病临床证据的老年原发性高血压左室肥厚患者的室性心律失常及心肌缺血的发生率增加 ,两者的昼夜节律变化基本相同     

Left ventricular structural characteristics in unilateral renovascular hypertension and primary aldosteronism

To assess the importance of the renin-angiotensin system and plasma volume as determinants of hypertensive left ventricular hypertrophy and its anatomy, patients with unilateral renovascular hypertension and primary aldosteronism were studied by echocardiography. Blood pressure, age and sex were matched as closely as possible. The 19 patients with unilateral renovascular hypertension and the 19 patients with primary aldosteronism were similar in age, sex and blood pressure (168 +/- 19/97 +/- 11 and 163 +/- 17/99 +/- 10 mm Hg, respectively), but plasma volume was increased in the patients with primary aldosteronism. Interventricular septal thickness, left ventricular posterior wall thickness, left ventricular mass index and relative wall thickness did not differ between the 2 groups of patients. There was a significant correlation between the level of systolic blood pressure and either left ventricular mass index (r = 0.34, p less than 0.05) or relative wall thickness (r = 0.58, p less than 0.001) in both groups of patients. Left ventricular end-diastolic dimension index was increased in the patients with primary aldosteronism compared with those with unilateral renovascular hypertension (3.2 +/- 0.4 vs 2.9 +/- 0.3 cm/m2, p less than 0.02). When confined to the patients with systolic pressure greater than or equal to 150 mm Hg, relative wall thickness was significantly increased in the patients with unilateral renovascular hypertension. Patients with primary aldosteronism and unilateral renovascular hypertension of similar blood pressure levels, age and sex have almost identical degrees of left ventricular hypertrophy and anatomy. In contrast, the patients with primary oldosteronism had increased left ventricular dimension index.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impaired left ventricular functional reserve in hypertensive patients with left ventricular hypertrophy

To determine whether patients with hypertension and especially those with left ventricular hypertrophy have subtle changes in cardiac function, we measured the increase in left ventricular ejection fraction and in systolic blood pressure to end-systolic volume index ratio with exercise in 40 hypertensive patients and 16 age-matched normotensive volunteers. Twenty-two hypertensive patients without hypertrophy had normal end-systolic wall stress at rest and exercise responses. In contrast, the 18 patients with echocardiographic criteria for left ventricular hypertrophy demonstrated a significant increase in end-systolic wall stress at rest compared with normal subjects (69 +/- 16 vs. 55 +/- 15 10(3) x dyne/cm2, p less than 0.05) despite having normal resting left ventricular size and ejection fraction. In patients with left ventricular hypertrophy, the increase in ejection fraction with exercise was less than in the normotensive control subjects (7 +/- 7 vs. 12 +/- 8 units, p less than 0.05), and delta systolic blood pressure to end-systolic volume with exercise was reduced (3.3 +/- 3.8 vs. 8.3 +/- 7.7 mm Hg/ml/m2, p less than 0.05). The hypertensive patients with hypertrophy displayed a shift downward and to the right in the relation between systolic blood pressure to end-systolic volume ratio and end-systolic wall stress compared with control subjects and hypertensive patients without left ventricular hypertrophy. Thus, hypertensive patients with left ventricular hypertrophy by echocardiography and normal resting ejection fraction exhibit abnormal ventricular functional responses to exercise. This finding may have implications in identifying patients at higher risk for developing heart failure.     

Exercise-induced ST-segment depression and myocardial ischemia in patients with hypertrophic cardiomyopathy: myocardial scintigraphic study

OBJECTIVES: Patients with hypertrophic cardiomyopathy (HCM) sometimes develop myocardial ischemia during exercise in the absence of coronary lesions. The relationship between myocardial ischemia and ST-segment depression was investigated during exercise testing in patients with HCM. METHODS: Regional hypoperfusion and/or transient left ventricular cavity dilation, a parameter of subendocardial hypoperfusion, were assessed on exercise 99mTc-tetrofosmin myocardial scintigraphy in 42 patients with non-obstructive HCM. The scintigraphic results were further correlated with the ST-segment responses to exercise. RESULTS: Regional hypoperfusion or transient left ventricular cavity dilation were observed in 19 (45%) or 16(38%)patients with HCM, respectively. The incidence of ST-segment depression > or = 0.1 mV during exercise testing was similar in HCM patients with regional hypoperfusion, with transient left ventricular cavity dilation, and without hypoperfusion (42%, 38%, 38%, p = 0.95). Furthermore, exercise-induced ST-segment depression > or = 0.1 mV occurred similarly irrespective of symptoms, exercise tolerance, the degree or the site of hypertrophy, or the presence or absence of resting ST-segment depression. CONCLUSIONS: ST-segment depression during exercise testing was common in patients with HCM, but seems to be an unreliable marker of myocardial ischemia as assessed by exercise scintigraphy.     

Left ventricular remodeling impairs coronary flow reserve in hypertensive patients

BACKGROUND : In arterial hypertension, changes in both left ventricular mass and geometry may occur. Concentric left ventricular remodeling (i.e. an increased wall thickness relative to end diastolic diameter) has been implicated as an independent cardiovascular risk factor in hypertensive patients. The influence of concentric remodeling on the coronary microcirculation is not known. OBJECTIVE : To investigate the impact of left ventricular geometry on coronary flow reserve in patients with arterial hypertension and angiographically normal coronary arteries. METHODS : Following exclusion of coronary artery disease by cardiac catheterization, coronary flow reserve (dipyridamole, 0.5 mg/kg body weight intravenously; argon gas-chromatographic method) was measured in 49 patients with arterial hypertension and in six age-matched controls. Hypertensive patients were grouped by echocardiographic findings according to left ventricular mass and relative left ventricular wall thickness (i.e. left ventricular posterior wall plus septal thickness divided by end diastolic diameter): seven patients had normal left ventricular mass and geometry, 19 had eccentric hypertrophy (i.e. normal relative wall thickness but increased mass), concentric remodeling (i.e. normal mass but increased relative wall thickness) was present in nine patients, and 14 patients had concentric hypertrophy. RESULTS : There was a marked reduction in coronary flow reserve in all hypertensive groups as compared with control values (4.2 +/- 0.5). Within the hypertensive subgroups, the coronary flow reserve was differentially reduced in the following rank order: concentric remodeling (2.0 +/- 0.7) approximately concentric hypertrophy (2.3 +/- 0.8) < eccentric hypertrophy (2.9 +/- 0.6) mu normal geometry (2.7 +/- 0.4). Multi-factorial regression analysis showed that the relative wall thickness but not left ventricular mass was independently linked to the coronary flow reserve. CONCLUSIONS : Concentric left ventricular remodeling is an independent predictor of the coronary flow reserve in hypertensive patients with chest pain and normal coronary angiogram. The impairment of the coronary microcirculation may contribute to the excess cardiovascular event rate associated with hypertensive concentric left ventricular remodeling.     

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.     

Determination of right ventricular wall thickness in systole and diastole. Echocardiographic and necropsy correlation in 32 patients.

To show that right ventricular wall thickness (RVWT) measurements can be made with precision by echocardiography, we correlated these measurements with those obtained at necropsy in 32 terminal patients. The correlation between the echocardiographic diastolic right ventricular wall thickness (mean 4.0 +/- 1.62 mm) and the necropsy measurement (mean 4.3 +/- 1.52 mm) was good (r = 0.83) in all 32 patients with normal or increased right ventricular wall thickness at necropsy. In 19 patients without necropsy evidence of right ventricular hypertrophy (RVWT less than or equal to 4 mm), the mean diastole and systolic right ventricular wall thickness were 3.0 +/- 0.92 mm and 5.1 +/- 1.64 mm, respectively. In 13 patients with necropsy evidence of right ventricular hypertrophy (RVWT greater than or equal to 5 mm), the mean diastolic and systolic right ventricular wall thicknesses were 5.3 +/- 1.56mm and 8.2 +/- 1.88 mm, respectively. We conclude that technically satisfactory echocardiograms of the right ventricular wall thicknesses. Echocardiography can reliably estimate the diastolic wall thickness and may be helpful in the evaluation of right ventricular hypertrophy.     

Influence of hypertension with minimal hypertrophy on diastolic function during demand ischemia

Hearts with advanced pressure-overload hypertrophy from systemic hypertension have been shown to have an increased susceptibility to the development of diastolic dysfunction in response to tissue hypoxia and ischemia. It is not known if this propensity to develop diastolic dysfunction in response to ischemia is dependent on the presence of a substantial increase in left ventricular mass, or alternatively, is characteristic of hearts subjected to mild chronic hypertension early in the development of cardiac hypertrophy. We tested the hypothesis that systemic hypertension associated with mild left ventricular hypertrophy increases the susceptibility to the development of diastolic dysfunction in response to demand ischemia. The effects of demand ischemia (6 minutes) were studied in hearts from New Zealand white rabbits with chronic systemic hypertension produced by the one-kidney, one-wrap method (n = 15) and compared with age-matched, sham-operated control rabbits (n = 11) with similar left ventricular mass (5.4 +/- 0.2 vs. 5.4 +/- 0.3 g, respectively). The hearts were studied using an isolated, isovolumic (balloon in left ventricle) preparation with absent pericardium that was perfused with fresh whole blood. At baseline, coronary perfusion pressure was 100 mm Hg with comparable coronary flow per gram left ventricular weight; the hearts were paced at a physiological rate of 3 Hz, and the left ventricular balloon volume was adjusted to achieve a left ventricular end-diastolic pressure of 15 mm Hg in both groups. Left ventricular balloon volume was similar in both groups and volume was thereafter held constant. At baseline, left ventricular systolic pressure (114 +/- 4 vs. 95 +/- 3 mm Hg, p less than 0.001) and developed pressure (18.9 +/- 1.2 vs. 15.1 +/- 0.9 mm Hg/g, p less than 0.05) were higher in the hearts from the hypertensive group in comparison with the control group. During the first minute of global ischemia produced by reducing coronary perfusion pressure from 100 to 20 mm Hg, there was an immediate fall in left ventricular systolic pressure in both groups without an increase in diastolic pressure. In response to the superimposition of pacing tachycardia (heart rate, 6 Hz) during the remaining 5 minutes of the period of ischemia, left ventricular developed pressure was comparable. However, isovolumic left ventricular end-diastolic pressure (measured during long diastoles obtained with transient cessation of pacing) rose to a significantly higher level in the hearts from hypertensive rabbits than in those from the control rabbits (29 +/- 3 vs. 18 +/- 2 mm Hg, p less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)     

Coronary vasodilator capacity and epicardial vessel remodeling in physiological and hypertensive hypertrophy

The aim of this study was to compare resting coronary flow velocity, determinants of myocardial oxygen demand, and coronary vasodilator capacity in subjects with physiological, exercise-induced, and hypertensive left ventricular hypertrophy. Sixteen healthy sedentary men, 16 endurance athletes, and 16 hypertensive subjects (mean+/-SEM for left ventricular mass index: 94.9+/-5.5, 184.6+/-8.4, 154.4+/-9.5 g/m(2), respectively) were studied by transesophageal and transthoracic Doppler echocardiography. Coronary flow velocity in left anterior descending artery and cross-sectional area of left main artery were assessed at rest and during dipyridamole-induced vasodilation. Myocardial oxygen demand was estimated through rate-pressure product, left ventricular wall stress, and inotropic function. Coronary flow reserve and minimum coronary resistance were comparable to those of sedentary men in athletes (mean+/-SEM: 3. 23+/-0.16 versus 3.60+/-0.18 and 0.96+/-0.06 versus 1.04+/-0.04 mm Hg. s. cm(-1)), while in hypertensive subjects they were decreased and increased, respectively (mean+/-SEM: 2.31+/-0.08 and 1.21+/-0.10 mm Hg. s. cm(-1); P:<0.05 for both). Resting flow velocity was directly related to rate-pressure product in sedentary men and athletes and also to wall stress in athletes, while these correlations were absent in hypertensives. Dilation of left main artery after dipyridamole was significantly higher in athletes than in sedentary men and hypertensive subjects (mean+/-SEM for area change: 32.9+/-3.7% versus 12.8+/-2.5% and 6.4+/-3.3%; P:<0.05 and 0.01). These data indicate that vasodilator capacity of coronary microcirculation is not impaired in athletes with physiological hypertrophy, in contrast to hypertensive patients. The relationship between resting flow velocity and determinants of oxygen demand is preserved in physiological hypertrophy but missing in hypertensive hypertrophy. Furthermore, the vasodilator capacity of coronary macrocirculation is also enhanced in exercise-trained subjects.     

The effect of cardiac hypertrophy on the coronary collateral circulation

We have previously shown that dogs with renal hypertension and left ventricular hypertrophy have larger infarcts (per risk area size) than do control animals. A potential explanation for this is that collateral resistance is higher in these dogs. Paradoxically, previous postmortem studies in human hearts with left ventricular hypertrophy have suggested that coronary collaterals are actually increased in this condition. To test the hypothesis that left ventricular hypertrophy is associated with alterations in coronary collateral resistance, studies were performed in dogs with renal hypertension and left ventricular hypertrophy and in patients with aortic valvular disease at the time of cardiac surgery. With an isolated, adenosine-vasodilated, blood-perfused cardiac preparation, collateral and normal zone pressure-flow relationships were established by means of radioactive microspheres in nine dogs with renal hypertension and left ventricular hypertrophy and in 17 controls. Collateral resistance calculated from these pressure-flow relationships were similar in both groups (4.0 +/- 0.7 in dogs with renal hypertension and left ventricular hypertrophy and 3.9 +/- 0.4 mm Hg/ml/min/100 g in controls). In addition, normal zone resistance was not different between groups (transmural resistances 0.17 +/- 0.01 in controls and 0.18 +/- 0.02 in dogs with renal hypertension and left ventricular hypertrophy. In five patients with aortic valve disease, left ventricular hypertrophy, and normal coronary arteries and in six patients without left ventricular hypertrophy who had normal left anterior descending coronary arteries, a 7 MHz suction-mounted echo transducer was used to monitor systolic wall thickening during transient occlusions of the left anterior descending artery at the time of cardiac surgery. Because noncollateralized myocardium ceases to contract promptly after coronary occlusion, this approach provides an indirect index of collateral perfusion. Twenty seconds after the onset of coronary occlusion, systolic thickening had markedly decreased in both groups (15 +/- 10% of control values in nonhypertrophied hearts and 10 +/- 10% in hearts with left ventricular hypertrophy; p = NS between groups). Thus the severity of contraction abnormality induced during transient coronary occlusion in these two groups of patients was similar, suggesting that the degree of severity of ischemia was comparable between the two groups. We conclude that collateral resistance is not altered by hypertension and left ventricular hypertrophy and that left ventricular hypertrophy in patients is not associated with functional evidence of an enhanced collateral circulation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Evaluation of norepinephrine content in the myocardium in hypertensive patients with left ventricular hypertrophy]

The sympathetic nervous system seems to be a non hemodynamic factor involved in the development of hypertension and in left ventricular hypertrophy determinism. The aim of this study was to estimate the myocardial norepinephrine content in essential hypertensive patients, using a reliable radio-iodinated marker of norepinephrine: the 123I-meta-iodobenzylguanidine (123I-meta-iodobenzylguanidine). Eight male and female hypertensive patients with left ventricular hypertrophy and average age of 52 +/- 9 years underwent a resting, ambulatory and effort blood pressure measure. Echocardiographic parameters allowed measure of left ventricular mass index (according to Devereux, and we considered left ventricular hypertrophy as left ventricular mass index greater than 120g/m2. Plasma norepinephrine is measured at rest. Cardiac and mediastinal radioactivity is detected 4 h after a 4mCi i.v. injection of 123I-meta-iodobenzylguanidine and meta-iodobenzylguanidine myocardial uptake is definite as the cardiac/mediastinal ratio (N:1.78 +/- 0.19). Meta-iodobenzylguanidine-myocardial uptake average value of hypertensive patients was 1.89 +/- 0.19 (1.63 to 2.25) without statistical difference to control subjects. We found a significative correlation between meta-iodobenzylguanidine myocardial uptake and effort systolic blood pressure variation in one hand, and with heart rate increase with effort in the other hand. There is no correlation between meta-iodobenzylguanidine-myocardial uptake and left ventricular mass index or ambulatory blood pressure. In hypertensive patients with left ventricular hypertrophy, meta-iodobenzylguanidine myocardial uptake is normal or high, in agreement with experimental data in SHRs, model of human essential hypertension. Therefore myocardial scintigraphy with 123I-meta-iodobenzylguanidine can appreciate cardiac norepinephrine content in humans.