The distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy: comparison to athletes and hypertensives

Cross-sectional echocardiogaphy was performed in 134 patientswith hypertrophic cardiomyopathy and 75 with secondary leftventricular hypertrophy (57 hypertensives and 18 athletes) todetermine the diagnostic sensitivity and specificity and predictivevalue of the pattern of left ventricular hypertrophy. Myocardialwall thickness was assessed in the anterior and posterior septum,free wall and posterior wall in both the upper and lower leftventricle. All patients had at least one region exceeding 2SD from normal (>l-4cm). Asymmetrical septal hypertrophy)septum to posterior wall ratio 1.5: 1 in the upper or lowerleft ventricle) was found in 75 patients with hypertrophic cardiomyopathy(56%), 11 hypertensives (18%) and 4 (22%) athletes. This patternwas more common in patients with primary compared to secondaryleft ventricular hypertrophy (P<0.01). Distal ventricularhypertrophy was only seen in patients with hypertrophic cardiomyopathy(10%). Symmetrical left ventricular hypertrophy was demonstratedin 45 patients with hypertrophic cardiomyopathy (34%), 50 hypertensives(82%) and 14 athletes (78%). This pattern was significantlymore common in patients with secondary left ventricular hypertrophy(P<0.01). Amongst those with symmetrical hypertrophy, patientswith hypertrophic cardiomyopathy had more severe hypertrophywhile the athletes had larger left ventricular cavity size.Asymmetrical septal hypertrophy was the most sensitive (56%)and distal ventricular (100%) the most specific pattern forthe diagnosis of hypertrophic cardiomyopathy with a predictivevalue of 83 and 100% respectively. Symmetrical left ventricularhypertrophy was 81% sensitive and 66% specific with a predictivevalue of 58% for the diagnosis of secondary hypertrophy. Inconclusion, the pattern of hypertrophy was of only moderatepredictive value in differentiating primary from secondary leftventricular hypertrophy.     

Cardiac hypertrophy in diabetic nephropathy: an echocardiographic study

Echocardiography was used to study the prevalence and severity of left ventricular hypertrophy in patients with established diabetic nephropathy (persistent proteinuria for at least 2 y plus severe retinopathy). Fifteen patients had mild renal impairment (serum creatinine less than 150 mumol l-1), 14 patients had moderate renal impairment (serum creatinine 150-400 mumol l-1), and 20 patients had severe renal impairment (serum creatinine greater than 400 mumol l-1). Thirty-six of the 49 (73%) were on anti-hypertensive treatment, despite which mean blood pressure was 161 +/- 25/89 +/- 9 (+/- SD) mmHg. Left ventricular hypertrophy was demonstrated in 42 of the 49 patients (85%), and increased in severity with increasing renal impairment. Interventricular septal + left ventricular posterior wall thickness was 25 +/- 3 mm in those with mild renal impairment, 28 +/- 6 mm in those with moderate renal impairment and 30 +/- 4 mm in those with severe renal impairment. The most severe left ventricular hypertrophy was seen in the Afro-Caribbean patients. Left ventricular hypertrophy was present even in those with marginally raised blood pressure and was related to age and serum creatinine but not to present blood pressure or duration of proteinuria.     

Mitral valve abnormalities in decedents of sudden cardiac death due to hypertrophic cardiomyopathy and idiopathic left ventricular hypertrophy

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An initial study on left ventricular diastolic function in patients with hypertrophy cardiomyopathy using single-beat, real-time, three-dimensional echocardiography

Objectives To assess the regional diastolic function in patients with hypertrophic cardiomyopathy (HCM) by using single-beat, real-time, three-dimensional echocardiography (RT-3DE). Methods Sixty-five patients with HCM in sinus rhythm together with fifty age- and gender-matched normal controls were studied by two–dimensional echocardiography (2DE) and RT-3DE. The parameters analyzed by RT-3DE included: left ventricular (LV) volumes, left ventricular ejection fraction (LVEF), end diastolic sphericity index (EDSI), diastolic dyssynchrony index (DDI), dispersion end diastole (DISPED), and normalized 17 segmental volume-time curves. Results LVEF was slightly lower evaluated by RT-3DE compared with 2DE (63.2 ± 6.8% vs. 59.1 ± 6.4%, P < 0.0001). Normal subjects had relatively uniform volumetric curves for all LV segments. In HCM patients, the segmental volumetric curves were dyssynchronous. Increased DDI and DISPED in end diastole were observed in patients with HCM (9.95 ± 3.75, 41.76 ± 17.19, P < 0.0001), not all abnormal volumetric segments occurred in the hypertrophic regions. Conclusions Patients with HCM have presented regional diastolic dyssynchrony in the diastole phase, and this preclinical lesion can be recognized by single-beat RT-3DE.     

Prevalence of left ventricular hypertrophy in Type I diabetic patients with diabetic nephropathy

Summary The increased mortality of patients with diabetic nephropathy is mainly due to cardiovascular disease and end stage renal failure. Left ventricular hypertrophy is an independent risk factor for myocardial ischaemia and sudden death. The aim of our cross-sectional study was to evaluate left ventricular structure and function in Type I (insulin-dependent) diabetic patients with diabetic nephropathy. M-mode and Doppler echocardiography were done on 105 Type I diabetic patients with diabetic nephropathy [61 men, age (means ± SD) 44 ± 9 years, and albuminuria [median(range)] 567(10–8188) mg/24 h, serum creatinine 109 (53–558) μmol/l], and 140 Type I diabetic patients with persistent normoalbuminuria [79 men, 47 ± 10 years, urinary albumin excretion rate 8 (0–30) mg/24 h, and serum creatinine 81 (55–121) μmol/l]. Patients with and without nephropathy were comparable with respect to sex, body mass index, and duration of diabetes. Arterial blood pressure was slightly higher in patients with nephropathy: 140/79 ± 17/9 mm Hg vs 134/78 ± 15/8 mm Hg, p < 0.01, and the majority of proteinuric patients received antihypertensive drugs, 84 vs 17 %, respectively, p < 0.001. Left ventricular mass index was increased in the nephropathic group (means ± SD) 100.6 ± 23.9 g/m² compared with the normoalbuminuric group 91.4 ± 21.9 g/m², p = 0.002. Left ventricular hypertrophy was found more often in patients with nephropathy 23 (14–31)% compared with patients with normoalbuminuria 9 (5–14)%, p < 0.005. Diastolic function, assessed by the ratio between the peak diastolic velocity and the peak atrial systolic velocity (E/A ratio) and isovolumic relaxation time, was reduced in patients with vs without nephropathy: 1.17 ± 0.29 vs 1.34 ± 0.32, and 81.7 ± 16.5 vs 74.6 ± 14.5, p < 0.001 and p = 0.002, respectively. Systolic function was about the same and normal in both groups. Our study suggests that an increase in left ventricular mass index and a decrease in diastolic function occurs early in the course of diabetic nephropathy. [Diabetologia (1999) 42: 76–80] Received: 16 April 1998 and in final revised form: 5 August 1998     

Diagnostic accuracy of a 2D left ventricle hypertrophy score for familial hypertrophic cardiomyopathy.

AIMS: To study the diagnostic value of a new 2D left ventricle hypertrophy (2D LVH) score in families with hypertrophic cardiomyopathy (HCM) in comparison with the conventional maximal wall thickness (MWT) measurement (>13 mm in adults), which is limited by a low sensitivity in relatives. METHODS AND RESULTS: The study was performed in 237 adults from genotyped families with HCM. Population A (derivation sample) comprised 109 adults and population B (validation sample) comprised 128 adults. MWT and 2D LVH scores (sum of thicknesses of four segments) were determined by echocardiography. Genotyping was the gold standard for diagnosis. In population A, a theoretical value for LVH score was determined in the healthy population by a multiple linear regression model including age, sex, and body surface area. An abnormal cut-off value was defined as an LVH score above a maximum theoretical value according to receiver operating characteristic analysis. Sensitivity and specificity were, respectively, 73 and 96% for 2D LVH score and 62.5 and 100% for MWT. Improvement of sensitivity was particularly important in adults <50 years of age (69 vs. 54%, respectively, P<0.04). These results were validated in population B: sensitivity and specificity of LVH score were, respectively, 75 and 96% in this sample and 67 and 97%, in the subgroup <50 years. In the latter, sensitivity of LVH score increased when compared with that of MWT (67 vs. 53%, P<0.03). CONCLUSIONS: The LVH score has a higher diagnostic value for HCM than the conventional criterion of MWT, particularly in young adults. This echographic parameter may be proposed as an alternative diagnostic criterion for familial screening.     

Increased myocardial contractility in short-term Type 1 diabetic patients: an echocardiographic study

Summary Cardiac function was investigated by echocardiography in 24 short-term Type 1 diabetic patients with a mean diabetes duration of 7 years (range 4–14 years) during conditions of ordinary metabolic control. Compared to 24 age and sex matched normal control subjects, measurements of myocardial contractility as left ventricular fractional shortening and mean circumferential shortening velocity were increased by 12% and 20% respectively. Another 8 Type 1 diabetic patients were examined during conditions of poor (hyperglycaemia and ketosis) and good metabolic control. Following improved glycaemic control, left ventricular fractional shortening and mean circumferential shortening velocity decreased by 16% and 24% respectively. Our findings show that short-term Type 1 diabetes is associated with increased myocardial contractility. Furthermore, this condition is related to the state of metabolic control.     

Intraventricular septal hypertrophy in type 1 diabetic patients with microalbuminuria or early proteinuria

To investigate whether the slightly increased blood pressure that occurs in early diabetic renal disease is associated with hypertensive left ventricular hypertrophy, M-mode echocardiograms were recorded in 11 non-diabetic control subjects and four groups of Type 1 diabetic patients. These were 15 patients without microvascular complications, 10 with microalbuminuria, 12 with early persistent proteinuria, and 8 with established renal impairment. Mean blood pressure was 133/80 mmHg (uncomplicated patients), 143/85 mmHg (microalbuminuria), 147/92 mmHg (early proteinuria) and 158/85 mmHg (renal impairment). Mean intraventricular septal width in the uncomplicated diabetic patients was 9.8 (SE 1.2) mm which did not differ from non-diabetic control subjects. Mean septal width was significantly greater in the other groups (microalbuminuria, 12.7 (1.1) mm, p less than 0.02; proteinuria, 12.0 (0.7) mm, p less than 0.05; renal impairment, 15.5 (1.8) mm, p less than 0.001). Left ventricular mass increased progressively between groups and was significantly increased in those with renal impairment (140 (21) vs 103 (5) g m-2 in uncomplicated patients, p less than 0.05). Septal width in the diabetic population not receiving antihypertensives (n = 37) was significantly correlated with systolic blood pressure (r = 0.45, p less than 0.005) which was the only variable independently related to septal width and ventricular mass. It appears that the slight increase in blood pressure that occurs in microalbuminuria and early proteinuria is frequently associated with hypertensive left ventricular hypertrophy.     

Pathophysiologic significance of left ventricular hypertrophy in dilated cardiomyopathy

Background and hypothesis: Patients with dilated cardiomyopathy (DCM) with left ventricular hypertrophy (LVH) have been found to have a better prognosis than patients without LVH. However, the pathophysiologic mechanism for that has not been investigated. We sought to clarify the pathophysiologic significance of LVH in DCM. Methods: We performed isoproterenol infusion echocar-diography (0.02 m?g/kg/min) in 17 patients with DCM, and measured plasma epinephrine and norepinephrine levels at rest and at the end of ergometer exercise in 14 of the 17 patients. Patients were classified into groups according to the presence (9 patients) (LVH+) or absence (8 patients) (LVH-) of LVH. Left ventricular hypertrophy was defined as an inter-ventricular thickness or posterior wall thickness ≥13 mm. Results: Although there was no significant difference between groups in fractional shortening at rest during isoproterenol infusion, fractional shortening was significantly higher in the LVH (+) group than in the LVH (-) group (29 ± 9 vs. 17 ± 8%;p<0.025). Although there was no significant difference in plasma norepinephrine level, it was significantly lower in the LVH (+) group than in the LVH (-) group (233 ± 169 vs. 519 ± 258 pg/ml;p<0.05) at the end point of the exercise. Conclusion: Systolic reserve, represented by the response to isoproterenol, is greater in patients with DCM with LVH than in those without LVH, and a lower plasma level of norepinephrine is needed to activate the myocardium during ex ercise in patients with DCM with LVH. This pathophysiologic characteristic could be one of the mechanisms which explain a better prognosis in patients with DCM with LVH.     

ACE inhibitors and regression of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a common condition and a powerful independent risk factor for coronary heart disease, congestive heart failure, and other cardiac morbidity. It is associated with the male sex and advancing age. Its most common cause is hypertension, and many antihypertensive agents induce regression of LVH. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reverse LVH by a mechanism as yet unknown. Reduction in afterload and other hemodynamic abnormalities by reduction of blood pressure is clearly a factor, but ACE inhibitors also block adrenergic action and other sympathetic nervous system influences, and the reduction in angiotensin II produces many effects. By inhibiting this potent vasoconstrictor and suppressing its degradation of the powerful vasodilator bradykinin, and by promoting sodium and water excretion, ACE inhibitors contribute to the restoration of normal ventricular function. Angiotensin II promotes protein synthesis in myocardial myocytes, and blocking this action may arrest the hypertrophic process. To determine the effect of angiotensin II on LVH and normalization of LV function, a study is now underway evaluating the effects of lisinopril, a new lysine analog of enalapril, and a diuretic agent in the treatment of hypertension LVH.     

Left ventricular hypertrophy in chronic kidney disease: A diagnostic criteria comparison

Background and aimsCKD patients have a high prevalence of LVH and this leads to an increase of cardiovascular risk. The aim of this study was to assess the prevalence of left ventricular hypertrophy (LVH) and left ventricular geometry in a group of 293 hypertensive patients with stage 2–5 chronic kidney disease (CKD), compared with 289 essential hypertensive patients with normal renal function.Methods and resultsAll patients underwent echocardiographic examination. Patients on stage 1 CKD, dialysis treatment, or with cardiovascular diseases were excluded. LVH was observed in 62.8% of patients with CKD and in 51.9% of essential hypertensive patients (P < 0.0001). We found increasingly higher left ventricular diameters, thicknesses, and mass from stage 2–5 CKD. Distribution of concentric and eccentric LVH was not very different between the two groups. However, after introducing mixed hypertrophy, the difference between the two groups group was disclosed (P = 0.027). Multiple regression analysis confirmed that the association between renal function and left ventricular mass (β ?0.287; P < 0.0001) was independent by potential confounders. Diastolic function was significantly worse in patients with CKD, especially in more advanced stages.ConclusionOur study confirms that LVH is highly prevalent in patients with CKD, especially by using the most recent cut off; in this population, LVH is often characterized by the simultaneous increase of wall thicknesses and diameters with negative effects on diastolic function.     

Myocardial stiffness and the timing difference between tissue Doppler imaging Ea and peak mitral valve opening can distinguish physiological hypertrophy in athletes from hypertrophic cardiomyopathy.

AIM: To differentiate between physiological and pathological left ventricular hypertrophy in athletes using echocardiography. METHODS AND RESULTS: Eleven patients with mild hypertrophic cardiomyopathy were compared against 17 international rowers with mild left ventricular hypertrophy, and 30 age matched controls. The time difference between peak Ea (Doppler tissue imaging) and peak mitral valve opening (using M-mode) was measured simultaneously. A novel index (E/Ea)/LVEDD, as a measure of left ventricular stiffness was recorded. In athletes the peak Ea preceded peak mitral opening by: median (interquartile range) 20 ms (10,20), control group 15 ms (0,30), compared with HCM where Ea followed peak mitral opening by 10 ms (0,20), P<0.0001. In athletes the index of left ventricular stiffness was lower than controls 1.2 (0.93,1.4) versus 1.5 (1.3,1.6), and HCM 2.2 (2.0,2.3), P<0.0001. CONCLUSION: Physiological hypertrophy can be differentiated from hypertrophic cardiomyopathy in athletes using the Ea-peak mitral opening difference, and our index of ventricular stiffness.     

Left ventricular apical hypertrophy emerged from the fourth-year post heart transplantation: Case report and literature review

Apical hypertrophic cardiomyopathy (AHCM) is a relatively rare phenotype of hypertrophic cardiomyopathy, which is characterized by focal thickening of the left ventricular (LV) apical myocardium, showing a spade-shaped shadow on the left ventricle. We present the case of a 59-year-old man who was found to have AHCM, is an asymptomatic orthotopic heart transplantation (HTx) patient. This rare and progressive case of LV apical hypertrophy emerged from the fourth year post surgery. We analyzed the etiology of this case and summarized the clinical manifestations and prognosis of AHCM following HTx by reviewing our case and the literature.     

Sex-differences in prevalence of electrocardiographic left ventricular hypertrophy in Type 2 diabetes: the Casale Monferrato Study.

AIMS Although left ventricular hypertrophy (LVH) defined by either standard 12-lead ECG or echocardiography strongly predicts cardiovascular mortality, its prevalence in Type 2 diabetes is largely unknown. We have assessed prevalence of ECG-LVH and its relationship with clinical and metabolic variables in an Italian population-based cohort of subjects with Type 2 diabetes. METHODS The study-base was 965 (61.3%) subjects with Type 2 diabetes of the population-based cohort living in Casale Monferrato (Italy). LVH was defined by ECG Cornell voltage-duration product. All measurements were centralized. RESULTS ECG-LVH was diagnosed in 165/965 subjects, giving a prevalence of 17.1% (95% CI 14.7-19.5). Large sex differences were found, with higher prevalence in women (23.5%, 19.9-27.0) than in men (8.4%, 5.6-11.0), even after adjustment for age, BMI and hypertension (OR 3.83, 95% CI 2.5-5.9). At the examination, subjects with ECG-LVH were older than those without it. Similar age- and sex-adjusted values of HbA(1c), plasma lipids, fibrinogen, uric acid and creatinine were found in the two subgroups. No differences in prevalence of hypertension, CHD, increased QT duration or dispersion, micro- and macro-albuminuria were found between subjects with ECG-LVH and those without it. In logistic regression analysis, variables independently associated with ECG-LVH, after age-adjustment, were sex and diastolic blood pressure. CONCLUSIONS: This population-based study shows: (i) a high prevalence of ECG-LVH in Type 2 diabetic subjects; (ii) 3-fold higher risk in women than in men, independently of age, BMI, and blood pressure; (iii) an independent association between ECG-LVH and diastolic blood-pressure. Screening for ECG-LVH in diabetic subjects is therefore recommended, particularly in diabetic women.     

依那普利逆转NIDDM合并高血压左心室肥厚效果的临床研究

目的　探讨依那普利逆转非胰岛素依赖型糖尿病 (NIDDM)合并高血压左室肥厚 (LVH)的疗效。　方法　对 30例NIDDM合并高血压LVH病人予以依那普利治疗 ,观察治疗前及治疗后 6个月的左室重量指数、E波峰速、A波峰速并与同期的 30例非NIDDM高血压LVH病人对比。　结果　发现依那普利可明显降低两组病人的左室重量指数 (P <0 0 5～P<0 0 0 1) ,并改善左室舒张功能 (P<0 0 5～P<0 0 0 1) ,但NIDDM组不及非NIDDM组明显。且NIDDM组逆转LVH的疗效与NIDDM病程呈负相关。　结论　提示依那普利能够逆转合并NIDDM的高血压LVH ,但逆转程度较无NIDDM者为弱。     

The effect of valsartan on regression of left ventricular hypertrophy in type 2 diabetic patients

AIM: The aim of the present study was to examine the effects of an angiotensin II receptor antagonist, valsartan, on echocardiographically proven left ventricular hypertrophy (LVH) in patients with type 2 diabetes. METHODS: Outpatients with type 2 diabetes mellitus were recruited at Niigata University Hospital. The left ventricular mass index (LVMI) was calculated by echocardiography. LVH was considered to be present if the LVMI was > 131 g/m(2) in males and > 100 g/m(2) in females. Patients with LVH received a low dose (40 mg/day) of valsartan for 12 months. This low dose had no clinical effect on blood pressure. RESULTS: Of the 38 patients who entered the study, 14 (36.8%) had LVH. After only 6 months of valsartan therapy, the mean LVMI decreased significantly, from 126.5 +/- 27.8 to 119.0 +/- 23.5 g/m(2) (p < 0.01 vs. baseline). Also, a significant decrease was observed after 12 months (116.5 +/- 30.9 g/m(2), p < 0.05 vs. baseline). Compared to baseline, there were no significant differences after treatment in body mass index, glycosylated haemoglobin (HbA(1c)), systolic blood pressure and diastolic blood pressure. CONCLUSIONS: In type 2 diabetic patients with LVH, treatment with a low dose of valsartan, an angiotensin II receptor antagonist, for 12 months, reduced LVMI, with no reduction in systemic blood pressure. This drug may be safely administered to type 2 diabetic patients with LVH. The long-term risk-reduction effects will have to be evaluated in further trials.