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We report the definite long-term natural history of a man with apical hypertrophic cardiomyopathy (ApHCM), who developed an apical aneurysm by the age of 60 years. At 33 years, his electrocardiogram (ECG) was nearly normal. T-wave inversions were first identified in leads V5–6 of an ECG at 36 years of age. Echocardiography first demonstrated a left ventricular (LV) lateral wall hypertrophy at 37 years of age. At 42 years, echocardiography showed the pattern of diastolic spade-like appearance of the LV cavity, confirming the ApHCM diagnosis. At 54 years, a late-peaking apical systolic gradient of 10mmHg (velocity: 1.6m/s) emerged. At 60 years, he had developed an apical aneurysm. Cardiac computed tomography revealed no significant major coronary artery stenosis. Thus, in our case, LV hypertrophy and apical high pressure in ApHCM advanced the formation of an apical aneurysm in the absence of coronary artery disease.

Most electrocardiographic criteria for left ventricular (LV) hypertrophy are relatively complex. They use absolute QRS voltage and often ST-T and P measurements to attain significant sensitivity and specificity. 1–6 New imaging methods are promising, but their restricted availability, radiation exposure and great cost make echocardiography the current standard for diagnosing LV hypertrophy. 7

Systemic hypertension usually develops in cyclosporinetreated heart transplant patients. 1 A major independent risk factor for cardiovascular events is left ventricular (LV) hypertrophy, 2 which may be expected with longstanding hypertension. We undertook this study to determine whether LV hypertrophy does develop in this setting, and if so, at what time after transplantation.

Recent reports suggest a role for serotonin in the pathogenesis of primary hypertension and left ventricular (LV) hypertrophy. In this study, we have induced LV hypertrophy by oral feeding of thyroxine at increasing dosages (150-450 micrograms/kg b.wt.) over a 5-week period. The effects of hyperthyroidism on cardiovascular parameters, blood and myocardial serotonin concentrations were assessed. Water-fed rats and formerly hyperthyroid recovered animals served as controls. Thyroxine caused a significant LV hypertrophy: hyperthyroid rats 2.19 +/- 0.16*; controls 1.65 +/- 0.13 g/kg b.wt. (mean +/- SD; *P less than 0.05). An almost complete regression of LV hypertrophy occurred in the recovery group (1.66 +/- 0.20 g/kg b.wt.) 3 weeks after cessation of thyroid hormone application. Thyroxine-treated animals showed a significant increase of serotonin blood levels (thyroxine rats: 2108 +/- 781*, recovery: 1132 +/- 726, controls: 705 +/- 480 ng/ml; *P less than 0.05). The concentrations of serotonin in left ventricular myocardium were increased after thyroid hormone application, whereas the highest levels were found in the recovery group (thyroxine rats: 139.1 +/- 30.4, recovery: 167.2 +/- 43.1, controls: 68.9 +/- 27.9 mg/ml homogenate). Serotonin-containing cells in the left ventricular myocardium were stained immunohistochemically. They were localized perivascularly and were assumed to represent tissue mast cells. In experimental hyperthyroidism the serotonin levels in blood and heart are increased possibly indicating an interaction of both hormones in thyroxine-induced cardiomyopathy.

The distribution of myocardial blood flow (MBF) was evaluated in pressure-induced LV hypertrophy of foxhounds. At the early stage of developing hypertrophy, i.e., 3 months after aortic banding (+ 53% LV weight) resting MBF and flow reserve were not significantly different from control hearts. One year after banding (+94% LV weight) myocardial flow reserve had clearly decreased. Acute coronary stenosis of 60 and 70% cross-sectional area resulted in a moderate fall of flow reserve in controls and hearts with early hypertrophy. In hearts with extensive hypertrophy the drop of poststenotic MBF was considerably greater affecting preferentially the subendocardium. The data suggest that myocardial blood flow was impaired before any signs of heart failure were observed. Furthermore a decrease of MBF may not be confined to forms of hypertrophy induced by renal and idiopathic hypertension.

Serial electrocardiographic and echocardiographic left ventricular (LV) studies were performed in 21 patients before and after aortic valve replacement (AVR) for chronic aortic regurgitation. Changes in voltage (SV1 + RV5-6) after AVR were assessed and evaluated relative to changes in LV mass. Muscle cross-sectional area (CSA) derived from echocardiographic dimension and wall thickness data was used as an index of LV muscle mass (LV hypertrophy greater than 10 cm2/m2). In 15 patients, voltage was reduced after AVR: Seven had normal voltage (48 +/- 17 mm to 25 +/- 6 mm, p less than 0.005) and eight still had increased voltage (61 +/- 17 mm to 40 +/- 4 mm, p less than 0.01). Patients with normal voltage had complete regression of hypertrophy by echocardiography (CSA decreased from 13 +/- 3 cm2/m2 to 9 +/- 1 cm2/m2, p less than 0.025), while those who had persistently increased voltage had incomplete regression (15 +/- 2 cm2/m2, p less than 0.001). Reduction in voltage generally occurred in the first 6 months after AVR. Three patients with unchanged voltage had evidence of paraprosthetic regurgitation and minimal change in CSA. Three other patients with voltage had evidence of paraprosthetic regurgitation and minimal change in CSA. Three other patients with persistent LV enlargement without paraprosthetic regurgitation had a severe intraventricular conduction delay. Data from 59 electrocardiographic-echocardiographic studies before and after AVR revealed a strong correlation (r = 0.81) between voltage and muscle CSA. After surgical correction of chronic aortic regurgitation, regression of LV hypertrophy can be assessed by serial electrocardiographic studies. These ECG data identify patients with complete, incomplete or no regression of LV hypertrophy.

Recent studies have shown that echocardiographically measured left ventricular (LV) mass is a strong predictor of cardiovascular morbidity in hypertension, possibly more important than blood pressure itself. Echocardiography has shown the left ventricle to be heterogeneous in hypertensive patients with regard to both the extent to which it uses increased myocardial mass or enhanced contractile performance to sustain the pressure load of hypertension and to the geometric patterns in which hypertensive LV hypertrophy occurs. The possible relationship of this heterogeneity of cardiac patterns in hypertension to differences in the etiology, pathogenesis, and prognosis of hypertension is a fruitful area for further investigation.

The left ventricle (LV) in hypertension has to pump against a chronically increased workload, so that a priori, we would expect LV hypertrophy (LVH) to be an inevitable consequence of hypertension. Yet the reported prevalence of LVH in human hypertension is relatively low, much more so than in animal models. The first part of this chapter considers possible reasons for the apparent paradox. Similarly, if we regard LVH as a physiological response to hypertension, LV myocardial function would be expected to be either normal or enhanced. But here too there is no consensus, with divergent conclusions based on studies in humans and animals. The experimental conditions under which LV function has often been compared, probably contribute to the above differences. For example, the performance of the normal and LVH heart have often been assessed under different loading conditions, as discussed in the second part of the chapter. However, there are problems of oxygen delivery through the coronary circulation, which ultimately set limits on myocardial performance. The last part of the chapter considers regression of myocardial hypertrophy during anti-hypertensive drug therapy and whether this should be an explicit therapeutic target in management.

The relationship between casual blood pressure and left ventricular (LV) mass has been reported to be fairly weak in hypertensive patients. In this study we analyzed this relationship using noninvasive devices to monitor blood pressure for 24 hours in ambulatory patients and M-mode echocardiography to determine LV mass. Among the 33 patients with hypertension, 21 had echocardiographic LV hypertrophy (LV mass greater than 250 g). Patients with LV hypertrophy did not differ significantly from patients without hypertrophy with respect to age or casual systolic or diastolic blood pressure. The averages of whole-day systolic and diastolic blood pressures were 146 +/- 17 (SD) over 90 +/- 12 and 136 +/- 16 over 89 +/- 12 mm Hg, respectively. The relationship between whole-day average systolic blood pressure and LV mass was significantly positive (r = 0.66, p less than 0.05) in patients without hypertrophy but was not significant in patients with LV hypertrophy (r = -0.24). Similarly, the relationship between whole-day average diastolic blood pressure and LV mass was significantly positive in the former group (r = 0.64, p less than 0.05) but significantly negative in hypertensive patients with LV hypertrophy (r = -0.67, p less than 0.01). Thus, blood pressure correlates positively with LV mass only in patients without cardiac hypertrophy. In hypertensive patients with LV hypertrophy, factors additional to the high blood pressure itself must participate in the regulation of LV mass.

To study the influence of left ventricular (LV) late diastolic filling on the A wave of the LV pressure, simultaneously recorded echocardiographic LV dimensions and high-fidelity LV pressure measurements were taken in 24 patients. Group 1 comprised eight patients without LV hypertrophy (LVH) and LV end-diastolic pressure (LVEDP) less than or equal to 13 mm Hg. Group 2 comprised 16 patients with LVH secondary to aortic stenosis, idiopathic hypertrophic subaortic stenosis, or hypertension and increased LVEDP. Patients in group 2 had significantly thicker left ventricles, decreased mitral E-to-F slopes, and larger A waves in the LV pressure curve. On the basis of end-diastolic chamber stiffness, we divided group 2 into two populations: 12 patients (group 2A) with end-diastolic chamber stiffness similar to that in group 1, and four patients (group 2B) with markedly elevated end-diastolic chamber stiffness. Patients in group 2A had a larger atrial contribution to LV filling than those with markedly abnormal stiffness (group 2B). Therefore, in LVH an increased A wave in the LV pressure may be related to either elevated end-diastolic chamber stiffness or augmented left atrial volume transport.

In previous echocardiographic studies of left atrial (LA) wall motion, investigators emphasized the importance of the motion of the posterior aortic root,1,2 which abuts on the most mobile portion of the left atrium and responds to volume changes within it. Although the posterior LA wall is considered less mobile, it can be examined directly. Patton et al3 observed that the mobility of the posterior inferior segment moved in a different direction from left ventricular (LV) wall motion and was considered feasible to avoid the inherent disadvantage of using an adjacent structure such as the posterior aortic root to assess cyclic LA wall changes. Therefore, we studied the effect of LV hypertrophy on LA wall motion during the passive phase of emptying in early diastole and during atrial systole.

The basis of every therapy in hypertensive heart disease is blood pressure normalization. However, blood pressure should be lowered through antihypertensive drugs, which can a) regress LV hypertrophy, b) increase myocardial perfusion and c) improve LV function depending on the stage of hypertensive heart disease. Such a step-care of hypertensive heart disease must not be understood as a therapeutic scheme, but should be considered as an attempt to cover the clinical therapy of common hypertensive cardiac complications.

To test the hypothesis that the capacity for left ventricular (LV) adaptation to volume overload might diminish with age, we examined the hemodynamics and degree of myocardial hypertrophy in response to aortic insufficiency in young adult (9 mo) and old (18 or 22 mo) Fischer rats. Before, immediately after, and at 2 and 4 wk after creating aortic insufficiency, LV and aortic pressures were measured using a catheterization technique. 4 wk after surgery, we measured aortic flow, and estimated the LV passive pressure-volume relationship and the degree of LV hypertrophy after killing. Immediately after the surgical creation of aortic insufficiency, both young and old rats showed similar elevation of LV end-diastolic pressure (from 4.8 +/- 0.6 to 12.0 +/- 1.5 mmHg in the young rats, P less than 0.01; from 4.9 +/- 0.4 to 11.0 +/- 0.7 mmHg in the old rats, P less than 0.01). In the young rats LV, end-diastolic pressure decreased to 8.0 +/- 1.0 and to 8.5 +/- 0.9 mmHg at 2 and 4 wk (P less than 0.05). In contrast, LV end-diastolic pressure at 2 (16.9 +/- 3.1 mmHg) and 4 wk (16.1 +/- 2.7 mmHg) in the old rats was even higher, compared with the values measured immediately after aortic insufficiency. At 4 wk, LV end-diastolic meridional wall stress (calculated from the in vivo LV end-diastolic pressure, and the pressure-volume relationship and muscle mass obtained after killing) was higher in the old rats than in the young rats. In the young rats, the diastolic pressure-volume relationship at 4 wk shifted to the right (P less than 0.01), and LV dry weight, LV dry weight/tibial length, and protein content of the LV myocardium increased by 26% (P less than 0.01), 24% (P less than 0.01), and 33% (P less than 0.01), respectively. However, old rats with aortic insufficiency did not show a significant change in the pressure-volume relationship, dry weight, or protein content at 4 wk. These results suggest that advanced age diminishes the capacity for LV hypertrophy in response to a volume overload, and this reduced LV hypertrophic response in the old rats resulted in persistent elevation of LV end-diastolic pressure and wall stress.

The noninvasive nature of echocardiographic/Doppler methods has allowed detailed assessment of cardiac anatomy and physiology in normal subjects and athletes, as well as accurate determination of left ventricular (LV) wall thickness and mass. 1,2 Recently, interest has developed in the use of Doppler recordings of mitral inflow to assess LV filling patterns in normal subjects, in conditioned athletes, and in various disease states associated with LV hypertrophy. 3–10 Several studies 6–9 have suggested that an increase in LV mass may be seen in certain highly trained athletes without any abnormalities in Doppler-derived LV filling parameters. This finding has engendered the term "physiologic" hypertrophy. However, little data are available on hearts of large body size athletes in whom LV mass is increased. In the present study highly trained aerobic athletes (professional basketball players) and nontrained normal subjects with large body size were evaluated by echocardiographic/Doppler techniques to determine whether increased LV mass and cavity size per se affect diastolic function when systolic function is normal.

Patients with hypertrophic cardiomyopathy (HC) often show substantial increases in left ventricular (LV) wall thickness or even de novo development of LV hypertrophy during childhood. To determine the utility of the electrocardiogram in reflecting such changes in LV mass, serial 12-lead electrocardiograms and 2-dimensional echocardiograms were analyzed in 38 children with HC. The period of evaluation ranged from 3 to 8 years (mean 5.5). Between the initial and most recent clinical evaluations, precordial and standard lead voltages did not change significantly in the study patients, including those showing evolution of LV hypertrophy by 2-dimensional echocardiography; furthermore, only 9 of the 38 patients (23%) showed any substantial change in the overall electrocardiographic pattern. However, the magnitude of electrocardiographic voltages at initial evaluation (age 11 +/- 4 years) showed a significant correlation with the extent of LV hypertrophy at the most recent evaluation as assessed by echocardiography (at age 16 +/- 4 years) (r = 0.65, p less than 0.001). Of note, each of the 7 patients who developed LV hypertrophy during the period of observation had distinct electrocardiographic abnormalities at the initial evaluation that preceded the appearance of LV hypertrophy on the echocardiogram. In conclusion, in children with HC and evolving LV hypertrophy, the electrocardiogram showed little change during the period of observation. However, electrocardiographic abnormalities may be the initial manifestation of HC, appearing even before LV hypertrophy is detectable by echocardiography. Hence, in patients with HC the electrocardiogram may provide advance evidence of morphologic changes that will subsequently occur and may describe the magnitude of LV hypertrophy ultimately achieved an average of 5 years later.(ABSTRACT TRUNCATED AT 250 WORDS)

Stratification of risk for cardiovascular events is a fundamental aspect of the assessment of hypertensive patients. The assessment of left ventricular (LV) hypertrophy is an important component of such stratification. The low prevalence of LV hypertrophy on the electrocardiogram (less than 3%) in patients with borderline or mild hypertension limits the utility of the electrocardiogram for stratification of risk in such patients. The high sensitivity (roughly 10-fold greater) and specificity of echocardiography for detection of LV hypertrophy and assessment of the severity and the various forms of such hypertrophy have prompted critical evaluation of the risk associated with such LV hypertrophy. Initial information suggesting considerable risk associated with echocardiographically detected increases in LV mass suggests significant clinical and public health importance of this tool. Further detailed cost-benefit analyses are needed to aid in assessing the role of echocardiography in the evaluation of patients with borderline and mild hypertension.

Recent echocardiography and angiographic studies have shown that hypertrophic obstructive cardiomyopathy (HOCM) is often associated with abnormal left ventricular (LV) relaxation and an abnormal diastolic filling pattern [1–3]. It was the purpose of this study to examine whether these abnormalities are only typical for this special type of LV hypertrophy or whether they can be found in other forms of LV hypertrophy as well [4].

Left atrial (LA) abnormality determined from precordial lead V1 was assessed by 2 observers as a criterion of left ventricular (LV) hypertrophy in the presence of right bundle branch block (BBS) in 23 patients. The presence of LV hypertrophy was confirmed from a postmortem cardiac partition technique and defined at 2 levels of confidence: probable and definite hypertrophy. Observers reliably differentiated between the hypertrophied and normal-sized ventricle in the presence of right BBB by using LA abnormality as an electrocardiographic criterion. When defined as definite hypertrophy, observer 1 correctly identified LV hypertrophy in 78% of the cases and observer 2 in 67% of the cases. False-positive results were present in 21% of cases by observer 1 and 14% by observer 2. Comparable results were achieved when a definition of probable hypertrophy was used. Observer performance of recognition of LA abnormality in this study was satisfactory with 91% agreement between observers. Our results are comparable and in some instances superior to conventional criteria commonly recommended to diagnose LV hypertrophy on the electrocardiogram without right BBB.

Considerable attention has properly been focused in recent years on electrocardiographs abnormalities in patients with essential hypertension. It has been well established that both voltage evidence of left ventricular (LV) hypertrophy and LV hypertrophy and strain are ominous risk factors. A better understanding of the strain pattern in patients with LV hypertrophy has arisen from experimental animal studies showing how an increase in cardiac mass can lead to myocardial ischemia and from clinical studies showing that the patient with LV hypertrophy and strain is at risk from myocardial ischemia as a consequence of both associated coronary artery disease and increased LV mass. All the clinical syndromes associated with myocardial ischemia are increased in patients with LV hypertrophy and therefore earlier recognition of both cardiac involvement and myocardial ischemia is likely to improve survival in this particularly high-risk group of patients.

To determine the accuracy of echocardiographic left ventricular (LV) dimension and mass measurements for detection and quantification of LV hypertrophy, results of blindly read antemortem echocardiograms were compared with LV mass measurements made at necropsy in 55 patients. LV mass was calculated using M-mode LV measurements by Penn and American Society of Echocardiography (ASE) conventions and cube function and volume correction formulas in 52 patients. Penn-cube LV mass correlated closely with necropsy LV mass (r = 0.92, p less than 0.001) and overestimated it by only 6%; sensitivity in 18 patients with LV hypertrophy (necropsy LV mass more than 215 g) was 100% (18 of 18 patients) and specificity was 86% (29 of 34 patients). ASE-cube LV mass correlated similarly to necropsy LV mass (r = 0.90, p less than 0.001), but systematically overestimated it (by a mean of 25%); the overestimation could be corrected by the equation: LV mass = 0.80 (ASE-cube LV mass) + 0.6 g. Use of ASE measurements in the volume correction formula systematically underestimated necropsy LV mass (by a mean of 30%). In a subset of 9 patients, 3 of whom had technically inadequate M-mode echocardiograms, 2-dimensional echocardiographic (echo) LV mass by 2 methods was also significantly related to necropsy LV mass (r = 0.68, p less than 0.05 and r = 0.82, p less than 0.01). Among other indexes of LV anatomy, only measurement of myocardial cross-sectional area was acceptably accurate for quantitation of LV mass (r = 0.80, p less than 0.001) or diagnosis of LV hypertrophy (sensitivity = 72%, specificity = 94%).(ABSTRACT TRUNCATED AT 250 WORDS)

To determine left ventricular (LV) structural and functional changes induced by ultraendurance exercise training, M-mode LV echograms and Doppler recordings of LV inflow velocity in 26 triathletes and 17 normal subjects were studied. All triathletes trained 20 to 40 hours/week in swimming, cycling and running for more than 2 years. Structurally, triathletes had normal LV systolic and diastolic cavity dimensions, but increased wall thickness (1.05 +/- 0.26 vs 0.80 +/- 0.27 cm in normal subjects, p less than 0.001), increased relative wall thickness, or h/R ratio (0.41 +/- 0.10 cm vs 0.33 +/- 0.11 cm in normal subjects, p less than 0.001), and increased LV mass (226 +/- 60 vs 143 +/- 54 g in normal subjects, p less than 0.001). LV mass correlated closely with mean exercise blood pressure during an 8-hour exercise test in 14 triathletes (r = 0.88). Systolic function at rest was similar in both groups, with no differences in fractional shortening or end-systolic stress. Diastolic LV function measured by digitized M-mode echo was similar in normal subjects and triathletes, with no differences in peak rates of cavity enlargement and wall thinning by echocardiogram. In contrast, the Doppler-derived ratio of early-to-late LV inflow velocities was slightly increased in triathletes (p less than 0.05). It is concluded that ultraendurance training produces a physiologic pattern of moderate pressure overload LV hypertrophy, in proportion to the hemodynamic load imposed during prolonged exercise. Unlike the abnormal hypertrophy of systemic hypertension, early diastolic function remains normal in the triathlete heart.

This study was undertaken to determine the prevalence and significance of diastolic left ventricular (LV) dysfunction in mild to moderate systemic hypertension. Rest and exercise equilibrium blood pool scintigraphy was performed in 39 hypertensive subjects (mean systolic blood pressure [BP] 156 +/- 14 mm Hg [+/- standard deviation]; mean diastolic BP 103 +/- 5 mm Hg) and 11 normal control subjects. These studies were analyzed for ejection fraction (EF), segmental wall motion, peak filling rate (PFR), time to PFR and filling fraction in the first third of diastole normalized for cycle length (first-third filling fraction). EF at rest was similar in the hypertensive patients and control subjects (0.63 +/- 0.09 versus 0.65 +/- 0.07); only 2 patients had a reduced EF. The EF response to exercise was normal in every hypertensive patient (increasing to a mean of 0.74 +/- 0.08); only 1 patient had asynergy. In contrast, even when the 2 patients with abnormal systolic function were excluded, each index of diastolic filling was significantly different from the control group. PFR was lower (2.29 +/- 0.49 vs 2.63 +/- 0.39 end-diastolic volumes per second [EDV/s], p less than 0.05), time to PFR was longer (199 +/- 47 versus 158 +/- 17 ms/s), p less than 0.01) and first-third filling fraction was smaller (0.38 +/- 0.11 vs 0.60 +/- 0.07, p less than 0.001). The latter index fell below the lowest normal value in 84% of the hypertensive patients. The degree of diastolic filling abnormality was not related to the patients' age, heart rate, BP, duration of systemic hypertension or systolic function.(ABSTRACT TRUNCATED AT 250 WORDS)

The R wave in precordial lead V4 or V5 usually has the greatest voltage in normal and abnormal electrocardiograms. Investigations before the advent of echocardiography showed that RV6 exceeding RV5 voltage appeared to be highly specific for left ventricular (LV) hypertrophy (irrespective of whether there was high, normal or low voltage).1,2 We investigated the correlation of the voltage ratio between RV6 and RV5 (RV6:RV5) with LV mass determined by echocardiography in a series of patients referred to the echocardiographic laboratory, and compared the results with 3 standard electrocardiographic methods for LV hypertrophy identification.

Despite improved patient detection and pharmacologic therapy, the effect of treatment of hypertension on mortality from coronary artery-related events remains unresolved. Left ventricular (LV) hypertrophy, a known consequence of hypertension, is associated with an excess mortality independent of other known cardiovascular risk factors. Recently, LV hypertrophy accompanying hypertension has been associated with ominous ventricular arrhythmias. However, it does not necessarily follow that regression of LV hypertrophy will reduce this increased mortality. Diastolic dysfunction, manifested by reduced ventricular distensibility of the hypertrophying left ventricle, appears to be an early characteristic of the hypertensive heart since echocardiographic techniques have demonstrated diastolic filling abnormalities in untreated essential hypertensives even before significant LV hypertrophy appears. Not all antihypertensive agents diminish LV mass and improve diastolic dysfunction. Certain sympatholytic agents, calcium antagonists, β-adrenergic blockers, and the angiotensin-converting enzyme inhibitors appear to diminish LV hypertrophy. However, future studies are needed to determine if these agents that appear to reverse findings of LV hypertrophy and improve diastolic dysfunction will also reduce risk of coronary artery disease and related events.

The response of the left ventricle (LV) during the development of spontaneous hypertension (SH) in rats was studied morphometrically at 21, 28, 35, and 45 days after birth and compared with that of normotensive (WK) controls. LV hypertrophy, varying from 24 to 27%, was characterized by the preservation of the volume fraction of capillary lumen and capillary luminal surface in the myocardium, as a result of capillary proliferation. From 21 to 45 days the number of capillaries per unit area of myocardium increased 68% in SH rats by the insertion in parallel of new capillary elements among the myocytes. This estimation was obtained by correcting the value of capillary density at 45 days for the amount of spreading produced by myocyte growth during this interval. On a similar basis capillary proliferation was only 24% in WK rats. Myocyte growth in experimental animals (151%) was achieved by a 77% enlargement in myocyte cross-sectional area (MCSA) and by a 42% lengthening of the cells. In controls myocyte expansion (124%) was the result of comparable increments in MCSA (47%) and myocyte length (53%).

An approach to the quantitative assessment of left ventricular (LV) diastolic stiffness in man has been developed utilizing strip-chart recordings of simultaneous ultrasonic LV dimensions, LV pressure, and electrocardiogram (ECG). In 23 patients without regional abnormalities of contraction, LV pressure, and LV internal diameter (D = distance between endocardial surfaces of LV posterior wall and septum at the plane of the mitral valve) were determined at the onset (P 1 , D 1 ) and peak (P 2 , D 2 ) of left atrial mechanical systole. In addition, left ventricular volumes, V 1 and V 2 , were calculated from D 1 and D 2 using a regression formula for end-diastolic volume previously determined from biplane angiographic studies. This allowed calculation of ΔP/ΔD and ΔP/ΔV associated with the "a" wave of the LV pressure trace, and these ratios were utilized as measures of LV stiffness late in diastole. Patients with LV hypertrophy by standard ECG criteria had much greater late diastolic stiffness (11 patients, ΔP/ΔD = 6.1 ± 1.1 mm Hg/mm, ΔP/ΔV = 1.0 ± 0.2 mm Hg/cc) than those without LV hypertrophy (12 patients, ΔP/ΔD = 1.8 ± 0.2 mm Hg/mm, ΔP/ΔV = 0.29 ± 0.04 mm Hg/cc, P < 0.001 for each ratio). Comparison of the stiffness ratios showed significant variation among patients with different disease states. Thus, late diastolic stiffness was highest in patients with aortic stenosis (three patients, ΔP/ΔD = 8.9 ± 2.9 mm Hg/mm, ΔP/ΔV = 1.5 ± 0.5 mm Hg/cc), lowest in mitral stenosis (four patients, ΔP/ΔD = 1.5 ± 0.5 mm Hg/mm, ΔP/ΔV = 0.23 ± 0.06 mm Hg/cc), and intermediate in patients with aortic regurgitation (three patients, ΔP/ΔD = 4.8 ± 0.7 mm Hg/mm, ΔP/ΔV = 0.83 ± 0.12 mm Hg/cc) and mitral regurgitation (three patients, ΔP/ΔD = 3.2 ± 0.7 mm Hg/mm, ΔP/ΔV = 0.5 ± 0.1 mm Hg/cc). It is concluded that the quantitative evaluation of LV diastolic stiffness obtained by this approach correlates well with the presence or absence of LV hypertrophy and with the underlying pathophysiology.

Aim. To assess the correlation between left ventricle remodeling induced by physical training with QTc duration in preadolescent professional football players. Material and methods. Ninety-four highly trained male footballers (mean aged 12,85±0,84) competing in the Serbian Football League (at least 7 training hours/ week) and 47 age-matched healthy male controls were enrolled in the study. Main outcome measures: They were screened by ECG and echocardiography at a tertiary referral cardio center. The control group had sedentary life style (less than 2 training hours/week). QTc values and left ventricle dimensions were compared in these two groups. Results. In all participants, normal values of QTc interval were registered. Mean QTc in athletes was significantly higher compared to non-athletes (419,89±13,07 msec vs 399,78±13,27 msec) (p

Background Cardiac magnetic resonance (CMR) is the gold standard imaging method to assess left ventricular mass (LVM), but M-mode echocardiography is more common during clinical practice. Proposed methods to normalize LVM to anthropometric measures provide different cut-off values for LV hypertrophy (LVH). We compare LVM assessed by echocardiography and CMR and evaluate the level of agreement for classification of LVH. Methods

We evaluated diastolic performance in 50 normal subjects and 50 patients with concentric left ventricular (LV) hypertrophy. Age-dependent normal values were determined for LV and left atrial (LA) acoustic quantification parameters. Pulsed wave Doppler echocardiography was also performed on all subjects. Patients with LV hypertrophy had higher peak velocities of atrial contraction and atrial contributions to filling. The acoustic quantification waveforms revealed lower rapid filling percentage of total filling and lower peak rapid filling rates. The LA acoustic quantification analysis confirmed the dependence on active atrial emptying in the patients with LV hypertrophy. There were significant correlations with age for most of the LV and LA acoustic quantification parameters. Acoustic quantification provided confirmatory results in subjects with an abnormal relaxation or restrictive Doppler pattern. In subjects with a normal Doppler pattern, the acoustic quantification was of added diagnostic value, identifying abnormalities in 77% to 80% of the patients. (J Am Soc Echocardiogr 1998;11:1027-35.)

The pattern of left ventricular (LV) filling has been recently studied using Doppler echocardiographic flow parameters. Abnormalities have been found in association with LV hypertrophy, myocardial infarction, aging and systemic hypertension.1 The effect of exercise and the attendant increase in stroke volume and heart rate on parameters of diastolic filling have not been studied, however, but may have importance as the application of exercise echocardiography increases. This study was performed to describe the normal changes that occur during upright exercise.

Background Two-dimensional strain (2D strain) has shown its usefulness for the assessment of right ventricular function. Normal values in elderly are still unknown and could have a prognostic value. Objectives To compare right ventricular (RV) regional and global longitudinal 2D strain (LS) in old healthy people to young healthy subjects and to patients with a pathological RV. Methods Old subjects without cardiac disease history were prospectively enrolled in a geriatric department after complete standard echocardiographic examination. Exclusion criteria were LV hypertrophy, LV dilation or dysfunction, significant valve disease, atrial fibrillation, pulmonary hepertension and right ventricular enlargement or dysfunction. 2D strain values were obtained from 3 segments of the RV lateral wall in 4 chamber apical view for longitudinal strain and were compared to values in young healthy people (from the medical staff) and to values in patients with Fallot disease or idiopathic pulmonary hypertension. Results 30 old subjects (25 females) with mean age of 85.8±3.94 yrs [75 to 95 yrs] (group 1), 30 young healthy subjects (19 females) with mean age of 29.2±4.77 yrs [17 to 39 yrs] (group 2) and 26 subjects with RV disease …were analyzed. The group 1 global LS values were significantly lower than those of group 2 and significantly higher than those of group 3. On the contrary tissue Doppler systolic wave (S’) showed no difference between group 1 and 2 and were significantly lower in group 3. Group 1 N=30 Group 2 N=30 Group 3 N=26 Global RV LS –23±7 * , † –27±5 14.8±5.2 RV S’ 13.9±3.0 † 12.8±2.7 9.4±2.7 * p † p Conclusion 2D strain allows RV function assessment and could note impairment this function in old people with “healthy” hearts not detected by conventional echocardiography and tissue Doppler velocities.

Dahl salt-sensitive rats fed with a high-salt diet (8% NaCI) progressively develop concentric LV hypertrophy (LVH, 11 weeks), which is followed by LV dilatation with pulmonary congestion (CHF, 18 weeks). To clarify modulation in cardiac energetics during the transition from LVH to CHF, we measured LV pressure-volume area (PVA) and myocardial oxygen consumption (MVO 2 ) in isolated, isovolumically contracting hearts from this animal model. Hearts were coronary-perfused with Tyrode's solution at 37°C and were paced at 3.33 Hz (perfusate Ca 2 +: 1 mM or 2 mM). The perfusion pressure was kept constant at 140 mmHg throughout the experiment. PO 2 in the perfusate and in the coronary effluent were continuously monitored with oxygen electrodes. The end-systolic pressure-volume relation (ESPVR) determined during the stepwise changes of the LV volume were fit by a binomial regression analysis, which provided a slope (Ees) and a volume intercept (V 0 ). Linear regression analysis of the MVO 2 -PVA relation determined a slope (A) and a MVO 2 intercept (B). Ca 2 + Ees V 0 A B mM mmHg.g.ml –1 mlxl0 –2 mlO 2 .mmHg –1 ·ml –1 x 10 –2 mlO 2 .beat –1 .g –1 LVH 1 1352 ± l25 1.97 ± 1.23 3.27 ± 1.45 1.80 ± 0.14 In = 5) 2 1853 ± 110 * 1.59 ± 0.98 2.10 ± 0.87 2.27 ± 0.20 * CHF 1 458 ± 98 † 7.33 ± 2.00 † 4.05 ± 115 1.18 ± 0.06 † (n = 4) 2 649 ± 148 * , † 5.60 ± 1.56 † 3.47 ± 0.86 1.52 ± 0.l5 * , † mean ± SEM. * p l 0.05 vs. Ca 2 + 1 mM, paired t-test † p l 0.05 vs. LVH, unpaired t-test During the transition from LVH to CHF, Ees was decreased and VO was increased These changes in inotropic state and in ventricular shape were associated with a decrease in the MVO 2 intercept, while the slope of MVO 2 -PVA relation was not altered. In conclusion, we confirm that the myocardial contractility and the ventricular remodeling occur during the transition from LVH to CHF in this animal model. Despite these changes, the oxygen cost of contractility does not change and the total energy cost of the remodeling myocardium might be preserved by reducing the expenditure for the non-mechanical process which includes the E-C coupling

to compare the effect of valsartan (Val) or ramipril (Ram) addition to amlodipine (Aml)/hydrochlorotiazide(HCTZ) combination on left ventricular (LV) mass in type 2 diabetic hypertensive patients with LV hypertrophy. a total of 180 mild to moderate hypertensive outpatients with well controlled type