Nondilated Left Ventricular Hypertrophy Research Articles

Prevalence and correlates of new-onset left ventricular geometric abnormalities in a general population: the PAMELA study.

We sought to evaluate new-onset abnormal LV (left ventricle) patterns and their correlates over a 10-year period in members of the general population enrolled in the Pressioni Arteriose Monitorate e Loro Associazioni study. The study included 817 patients with normal LV geometry at baseline evaluation having a readable echocardiogram at the end of follow-up. Cut-points for abnormal LV geometric patterns were derived from reference values of the healthy fraction of the Pressioni Arteriose Monitorate e Loro Associazioni population. Over a 10-year period 39% of participants progressed to abnormal LV geometric patterns as follows: LV concentric remodelling (15.2%), eccentric dilated left ventricular hypertrophy (LVH) (8.4%), concentric LVH (7.9%), eccentric nondilated LVH (6.8%), and concentric dilated LVH (0.7%). Age [odds ratio (OR): 1.039; 95% confidence interval (CI) 1.023-1.056, P < 0.0001], LV mass index (OR: 1.039; 95% CI 1.026-1.052, P < 0.0001), night-time SBP (OR: 1.024; 95% CI 1.005-1.043, P = 0.01), office SBP changes during follow-up (OR: 1.017 95% CI 1.007-1028, P = 0.001), and BMI (OR: 1.067; 95% CI 1.017-1.120, P = 0.009) emerged as key correlates of new-onset abnormal LV geometry. Age and LV mass index turned out to be strong determinants of all sub-types of LVH; whereas blood pressure, BMI, and sex exhibited a different predictive value across the various LV geometric patterns. Our study provides the first evidence that long-term changes from normal cardiac morphology toward abnormal LV geometry represent a clinically relevant phenomenon at the community level. From a practical perspective this finding reinforces the concept that life-style changes and pharmacologic treatment aimed to reduce over-weight/obesity and optimize blood pressure are of paramount importance for prevention of subclinical cardiac damage.

Do Combined Electrocardiographic and Echocardiographic Markers of Left Ventricular Hypertrophy Improve Cardiovascular Risk Estimation?

The authors estimated the risk of cardiovascular mortality associated with echocardiographic (ECHO) left ventricular hypertrophy (LVH) and subtypes of this phenotype in patients with and without electrocardiographic (ECG) LVH. A total of 1691 representatives of the general population were included in the analysis. During a follow-up of 211 months, 89 cardiovascular deaths were recorded. Compared with individuals with neither ECHO LVH nor ECG LVH, fully adjusted risk of cardiovascular mortality increased (hazard ratio [HR], 3.36; 95% confidence interval [CI], 1.51-7.47; P=.003) in patients with both ECHO-LVH and ECG-LVH, whereas the risk entailed by ECHO-LVH alone was of borderline statistical significance (P=.04). Combined concentric nondilated LVH and ECG-LVH, but not concentric nondilated LVH alone, predicted cardiovascular death (HR, 3.79; 95% CI, 1.25-11.38; P=.01). Similar findings were observed for eccentric nondilated LVH (HR, 3.37; 95% CI, 1.05-10.78; P=.04.). The present analysis underlines the value of combining ECG and ECHO in the assessment of cardiovascular prognosis related to abnormal left ventricular geometric patterns.

Risk of mortality in relation to an updated classification of left ventricular geometric abnormalities in a general population: the Pamela study.

We estimated the risk of cardiovascular and all-cause mortality associated with left ventricular geometric patterns, as defined by a new classification system proposed by the Dallas Heart Study, in 1716 representatives of the general population of Monza enrolled in the Pressioni Monitorate e Loro Associazioni (PAMELA) study. Cut-points for abnormal left ventricular geometric patterns were derived from reference values of the healthy fraction of the PAMELA population by combining left ventricular mass (LVM) index, left ventricular diameter and relative wall thickness. Death certificates were collected over an average 211 months follow-up period. During follow-up, 89 fatal cardiovascular events and 264 all-cause deaths were recorded. Concentric remodelling was the most common left ventricular geometric abnormality (9.4%) followed by eccentric nondilated left ventricular hypertrophy (LVH) (6.3%), concentric LVH (4.6%) and eccentric dilated LVH (3.5%). Compared with normal left ventricular geometry, concentric LVH [hazard ratio 2.20, 95% confidence interval (95% CI) 1.44-3.37, P < 0.0003], eccentric dilated LVH (hazard ratio 1.90, 95% CI 1.17-3.08, P = 0.009) and eccentric nondilated LVH (hazard ratio 1.57, 95% CI 1.07-2.31, P = 0.02) predicted the risk of cardiovascular mortality, after adjustment for baseline covariates, including ambulatory blood pressure. Similar findings were observed for all-cause mortality. Only concentric LVH maintained a significant prognostic value for both outcomes after adjustment for baseline differences in LVM index. The new classification system of left ventricular geometric patterns may improve mortality risk stratification in a general population. The risk is markedly dependent on LVM values; only concentric LVH provides a prognostic information beyond that conveyed by cardiac mass.

The relationship between left ventricular deformation and different geometric patterns according to the updated classification: findings from the hypertensive population.

We sought to investigate left ventricular mechanics in hypertensive patients with different geometric patterns by using two-dimensional (2DE) and three-dimensional (3DE) strain analysis. This cross-sectional study included 197 hypertensive individuals who underwent a complete 2DE and 3DE examination. We applied the new updated criteria of left ventricular geometry that considered left ventricular mass index, left ventricular end-diastolic diameter and relative wall thickness. According to this classification the individuals were divided into six groups: normal geometry, concentric remodelling, eccentric nondilated left ventricular hypertrophy (LVH), concentric LVH, dilated LVH and concentric-dilated LVH. Multidirectional 2DE and 3DE left ventricular strain decreased from the hypertensive patients with normal geometry, across the individuals with left ventricular concentric remodelling, eccentric nondilated LVH, to the patients with concentric LVH and dilated LVH patterns. The reduction of left ventricular systolic and early diastolic strain rates was noticed to be heading in the same direction, as well as the elevation of late diastolic strain rates. Left ventricular twist and torsion were increased in the participants with concentric and dilated LVH patterns. Reduced 2DE and 3DE strains were associated with concentric and dilated LVH patterns independent of demographic and clinical parameters. Left ventricular deformation in hypertensive patients is significantly impacted by left ventricular geometry. Concentric and dilated LVH patterns have the greatest unfavourable effect on 2DE and 3DE left ventricular mechanics. The updated classification of left ventricular geometry provides valuable and comprehensive information about left ventricular mechanical deformation and function in hypertensive population.

The influence of left ventricular geometry on left atrial phasic function in hypertensive patients

Objective. We aimed to investigate left atrial (LA) phasic function in hypertensive patients with different geometric patterns using two-dimensional (2DE) and three-dimensional (3DE) echocardiography. Methods. This cross-sectional study included 213 hypertensive subjects who underwent a complete 2DE and 3DE examination. The new updated criteria for left ventricular (LV) geometry, which consider LV mass index, LV end-diastolic diameter and relative wall thickness, were applied. According to this classification, the subjects were divided into six groups: normal geometry, concentric remodeling, eccentric non-dilated left ventricular hypertrophy (LVH), concentric LVH, dilated LVH and concentric-dilated LVH. Results. 2DE and 3DE LA volumes gradually increased from normal LV geometry to concentric and concentric-dilated LVH. LA reservoir and conduit functions, estimated by 2DE and 3DE LA total and passive emptying fractions, were decreased in subjects with concentric and concentric-dilated LVH. LA booster pump function was increased in patients with concentric, dilated and concentric-dilated LVH compared to subjects with normal LV geometry. The same results regarding LA phasic function were provided by 2DE strain analysis. Concentric, dilated and non-concentric dilated LVH were associated with LA enlargement independently of main demographic and clinical features. Conclusion. LV geometric patterns significantly influence LA phasic function. Concentric and dilated LVH patterns have the most prominent negative effect on LA enlargement assessed by both 2DE and 3DE.

Cardiovascular risk in relation to a new classification of hypertensive left ventricular geometric abnormalities.

In 2010, the Dallas Heart Study proposed an upgrade of the left ventricular geometric classification proposed in 1991, by using left ventricular mass combined with end diastolic volumes, and introducing the new categories of dilated left ventricular hypertrophy (LVH). We adopted the new method to test the prognostic impact of the left ventricular geometric patterns from the new classification. We evaluated baseline anthropometric, laboratory and echocardiographic parameters of 8848 hypertensive patients from the Campania Salute Network (53 ± 12 years, 56% male), free of prevalent cardiovascular disease, valve disease and with ejection fraction ≥50%. Cut points for left ventricular mass index, relative wall thickness and left ventricular end-diastolic dimension (cm/m) were derived from our historical normal reference population. Composite cardiovascular end-points were cardiac death, fatal and nonfatal myocardial infarction and stroke. Independent of confounders, eccentric dilated LVH, concentric nondilated LVH and concentric dilated LVH were associated with higher cardiovascular risk (hazard ratios between 2 and 9, all P < 0.01), mostly depending on the magnitude of LVM index. A volume load was present especially in dilated forms of LVH, the extent of which was important in the determination of harmful types of left ventricular geometry. Consideration of left ventricular dilatation in the evaluation of risk related to hypertensive left ventricular geometry reveals the importance of the extent of the volume load coexisting with the typical hypertensive pressure overload. At a given normal ejection fraction, the balance between the two hemodynamic components influences the shape of left ventricular geometric adaptation, the amount of left ventricular mass and the impact on prognosis.

Subclassification of left ventricular hypertrophy based on dilation stratifies coronary artery disease patients with distinct risk.

A new 4-tired classification of left ventricular hypertrophy (LVH) based on LV concentricity and dilation has been proposed; however, the association between the new categorization of LV geometry and outcomes in patients with coronary artery disease (CAD) is still unknown. All the 2297 patients with CAD included underwent echocardiographic examination prior to discharge. Left ventricular mass (LVM) was calculated, and left ventricular end-diastolic volume (EDV) was indexed by body surface area (BSA). Study cohort was divided into five groups according to LV geometry: (i) eccentric nondilated LVH (normal LVM/EDV((2/3)) and EDV/BSA) (n=129); (ii) eccentric dilated LVH (normal LVM/EDV((2/3)) with increased EDV/BSA) (n=222); (iii) concentric nondilated LVH (increased LVM/EDV((2/3)) with normal EDV/BSA) (n=441); (iv) concentric dilated LVH (increased LVM/EDV((2/3)) and EDV/BSA) (n=118); and (v) normal LV mass (n=1387). Dilated LVH was associated with a higher event rates of all-cause death (eccentric 13·1% vs. 3·1%; concentric 13·6% vs. 8·4%) and composite events (eccentric: 17·6% vs. 5·4%; concentric: 18·6% vs. 12·7%) compared with nondilated LVH. While eccentric nondilated LVH had comparable risk for adverse outcomes compared with normal LV mass (all-cause death: relative risk (RR) 0·68, 95% confidential interval (CI) 0·25-1·85; composite events: RR 0·75, 95% CI 0·36-1·58). Cox regression analyses showed that eccentric dilated LVH had the highest propensity to all-cause death (adjusted hazard ratio [aHR] 2·752 [95% CI 1·749-4·328], P<0·001) and composite events (aHR 2·462 [95% CI 1·688-3·592], P<0·001). In patients with CAD, dilated LVH and nondilated LVH provide distinct prognostic information. Eccentric nondilated LVH does not predict adverse outcomes.

Vascular changes in hypertensive patients with different left ventricular geometry

To evaluate vascular structural changes in hypertensive patients with different patterns of left ventricular geometry. From 250 untreated hypertensive patients who underwent ambulatory blood pressure monitoring and echocardiographic study, we selected four groups matched for sex, age, body mass index, smoking habits and serum lipid values: 25 hypertensive subjects with normal left ventricular geometry, 16 with concentric left ventricular remodeling, 26 with concentric left ventricular hypertrophy and 18 with eccentric non-dilated left ventricular hypertrophy. These patients underwent carotid ultrasonography to evaluate the intimal-medial thickness and lumen diameter, and venous occlusion plethysmography to record minimum forearm vascular resistance (an index of arteriolar structural changes). The intimal-medial thickness and minimum forearm vascular resistance were significantly higher (both P<0.05) in hypertensive subjects with concentric left ventricular remodeling (0.95 mm, 2.68 RU) and concentric left ventricular hypertrophy (0.96 mm, 2.71 RU) than in those with eccentric non-dilated left ventricular hypertrophy (0.81 mm, 2.36 RU) and normal left ventricular geometry (0.71 mm, 2.15 RU). There was no difference between hypertensive patients with concentric left ventricular remodeling and concentric left ventricular hypertrophy. The intimal-medial thickness and minimum forearm vascular resistance tended to be higher in hypertensive subjects with eccentric non-dilated left ventricular hypertrophy than in those with normal left ventricular geometry, but this difference did not attain statistical significance. This study shows that the spectrum of cardiac adaptation to hypertension is associated with a spectrum of vascular adaptation which might be related both to hemodynamic stimuli and differences in the expression or activity of vascular growth factors.

Determinants of ventricular ectopy in hypertensive cardiac hypertrophy

Left ventricular hypertrophy in arterial hypertension has repeatedly been documented to trigger or aggravate ventricular ectopy. To determine cardiovascular mechanisms underlying ventricular ectopy, we examined 53 hypertensive patients with mild to moderate nondilated left ventricular hypertrophy by 24-hour echocardiographic monitoring and two-dimensional (2-D)-guided M-mode echocardiography. Patients with more severe ectopy (Lown's class II to IV) were older and had greater increases in left ventricular mass, ejection fraction, velocity of circumferential fiber shortening, end-diastolic volume index, and left ventricular stroke work than patients with less severe ectopy (Lown's class 0 to I). Left ventricular mass, end-diastolic diameter, stroke volume, stroke work, ejection rate, velocity of circumferential fiber shortening, and fractional fiber shortening were enhanced in a subgroup with complex ventricular ectopy (multiform or paired premature ventricular beats or runs of ventricular tachycardia) when compared with a subgroup matched with respect to age, sex, body surface area, and mean arterial pressure, which had uniform monofocal ventricular beats occurring with a frequency of less than 10/hr only. Our data indicate that the frequency and severity of ventricular ectopy in patients with essential hypertension is determined by age, severity of left ventricular hypertrophy, chamber volume, and indices of contractility and pump function. Whether or not the pattern of ventricular ectopy will identify hypertensive patients with left ventricular hypertrophy who are at increased risk of sudden death remains to be determined.

Left ventricular hypertrophy. Relation of structure to diastolic function in hypertension.

Digitised M mode echocardiography was used to determine the relation between the degree of left ventricular hypertrophy and abnormalities of isovolumic relaxation and diastolic function. Fifty six patients with varying severity of non-malignant systemic hypertension without evidence of ischaemic heart disease, left ventricular dilation, or clinical heart failure were studied. In addition, 10 athletes with hypertrophy and 20 normal subjects were studied. Athletes and patients with moderate (systolic blood pressure 175 to 200 mm Hg) and severe hypertension (greater than 200 mm Hg) had a significant increase in left ventricular mass. Cavity dimensions were normal in hypertensive patients and increased in athletes. Systolic function was normal in all groups. Regardless of the degree of hypertrophy patients with hypertension had a prolonged isovolumic relaxation period and delayed mitral valve opening. Patients with hypertrophy also had a reduced rate and prolonged duration of rapid early diastolic dimension increase and posterior wall thinning. Athletes, however, who had an equivalent degree of hypertrophy to patients with moderate or severe hypertension had entirely normal function. Measurements of diastolic function were significantly correlated with wall thickness and left ventricular mass. These indices of hypertrophy, particularly posterior wall thickness and the sum of posterior wall and septal thickness, were positively correlated with the duration of isovolumic relaxation and delay in mitral opening and negatively with the peak rate of early diastolic dimension increase and wall thinning. Thus in hypertensive patients with non-dilated left ventricular hypertrophy there appears to be a relation between the degree of wall thickening and abnormalities of diastolic function.