Study on the Effect of Echocardiography in the Diagnosis of Hypertension with Left Ventricular Hypertrophy and Left Heart Failure

Background: Left ventricular hypertrophy (LVH) is an established risk factor for heart failure (HF). However, it is unknown whether LVH detected by electrocardiogram (ECG-LVH) is equivalent to LVH ascertained by cardiac magnetic resonance imaging (MRI-LVH) in terms of prediction of incident HF using risk prediction models like the Framingham Heart Failure Risk Score (FHFRS). Methods: This analysis included 4745 (mean age 61+10 years, 53.5% women, 61.7% non-whites) from the Multi-Ethnic Study of Atherosclerosis who were free of cardiovascular disease at the time of enrollment. ECG-LVH was defined using Cornell’s criteria while MRI-LVH was derived from left ventricular (LV) mass measured by cardiac MRI. Cox proportional hazard regression was used to examine the association between ECG-LVH and MRI-LVH with incident HF. Harrell’s concordance C-index was used to estimate the predictive ability of the FHFRS when either ECG-LVH or MRI-LVH were included as one of its components. The added predictive ability of ECG-LVH and MRI-LVH were investigated using integrated discrimination improvement (IDI) index and relative IDI. Results: ECG-LVH was present in 291(6.1%) while MRI-LVH was present in 499 (10.5%) of the participants. Over a median follow up of 10.4 years, 140 participants developed HF. Both ECG-LVH [HR (95% CI): 2.25(1.38-3.69)] and MRI-LVH [HR (95% CI): 3.80(1.56-5.63)] were associated with an increased risk of HF in multivariable adjusted models (Table 1). The ability of FHFRS to predict HF was improved with MRI-LVH (C-index 0.871, 95% CI: 0.842-0.899) when compared with ECG-LVH (C-index 0.860, 95% CI: 0.833-0.888) (p < 0.0001). To assess the potential clinical utility of using LVH-MRI instead of ECG-LVH, we calculated several measures of reclassification (Table 1), which were consistent with the statistically significantly improved C-statistic with MRI-LVH. Conclusion: Both ECG-LVH and MRI-LVH are predictive of HF when used in the FHFRS. Substituting MRI-LVH for ECG-LVH improves the predictive ability of the FHFRS.

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Heart valve disease, left ventricular hypertrophy, and heart failure: a lifelong relationship and continuing clinical responsibility

European Journal of Heart Failure ◽

10.1002/ejhf.2373 ◽

2021 ◽

Author(s):

Alan G Fraser ◽

Piotr Szymański

Keyword(s):

Heart Failure ◽

Left Ventricular Hypertrophy ◽

Heart Valve ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Valve Disease ◽

Heart Valve Disease ◽

Clinical Responsibility

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Compensatory hypertrophy and failure in gradual pressure-overloaded guinea pig heart

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.3.h1016 ◽

1989 ◽

Vol 257 (3) ◽

pp. H1016-H1024 ◽

Cited By ~ 2

Author(s):

F. M. Siri ◽

C. Nordin ◽

S. M. Factor ◽

E. Sonnenblick ◽

R. Aronson

Keyword(s):

Heart Failure ◽

Left Ventricular Hypertrophy ◽

Guinea Pig ◽

Ventricular Hypertrophy ◽

Significant Proportion ◽

Systolic Pressure ◽

Left Ventricular ◽

Compensatory Hypertrophy ◽

Guinea Pig Heart ◽

Ventricular Afterload

Left ventricular hypertrophy has been produced in the guinea pig by a procedure that gradually increases left ventricular afterload. A mildly constricting band was placed around the ascending aortas of very young guinea pigs (225–275 g). With growth to 500–1,000 g, left ventricular systolic pressure increased and left ventricular hypertrophy developed. In approximately 50% of these animals, the hypertrophy was associated with normal left ventricular function and with no unusual symptoms or evidence of heart failure. The other animals developed dyspnea, which appeared an average of 41 days after banding. Dyspneic animals had normal body weight, markedly increased right ventricular and lung weights, decreased left ventricular norepinephrine content, diminished maximum left ventricular pressure generating capacity, and a significantly higher incidence of left ventricular interstitial and perivascular fibrosis. These findings demonstrate that even when left ventricular overload is imposed gradually by banding the aortas of young animals, myocardial decompensation ultimately ensues in a significant proportion of such animals. The slow imposition of loading, the slow rate of decompensation, and the ability to identify animals in heart failure by clinical dyspnea make this model uniquely valuable for studies on the mechanisms of heart failure.

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Isosorbide Dinitrate, With or Without Hydralazine, Does Not Reduce Wave Reflections, Left Ventricular Hypertrophy, or Myocardial Fibrosis in Patients With Heart Failure With Preserved Ejection Fraction

Journal of the American Heart Association ◽

10.1161/jaha.116.004262 ◽

2017 ◽

Vol 6 (2) ◽

Cited By ~ 18

Author(s):

Payman Zamani ◽

Scott Akers ◽

Haideliza Soto‐Calderon ◽

Melissa Beraun ◽

Maheswara R. Koppula ◽

...

Keyword(s):

Heart Failure ◽

Left Ventricular Hypertrophy ◽

Ejection Fraction ◽

Myocardial Fibrosis ◽

Isosorbide Dinitrate ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Preserved Ejection Fraction ◽

Wave Reflections ◽

Patients With Heart Failure

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Electrocardiographic changes in patients with cardiac rhabdomyomas associated with tuberous sclerosis

Cardiology in the Young ◽

10.1017/s1047951103000507 ◽

2003 ◽

Vol 13 (3) ◽

pp. 258-263 ◽

Cited By ~ 12

Author(s):

Junko Shiono ◽

Hitoshi Horigome ◽

Seiyo Yasui ◽

Tomoyuki Miyamoto ◽

Miho Takahashi-Igari ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Left Ventricular Hypertrophy ◽

Tuberous Sclerosis ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Cardiac Rhabdomyoma ◽

Ventricular Cavity ◽

Electrocardiographic Changes

Background:Cardiac rhabdomyomas associated with tuberous sclerosis induce various abnormalities in the electrocardiogram. Electrocardiographic evidence of ventricular hypertrophy may appear if the tumour is electrically active. To our knowledge, electrocardiographic evidence of ventricular hypertrophy has been reported only in association with congestive heart failure. Follow-up studies of changes in electrocardiographic findings are also lacking.Methods:We studied 21 consecutive patients with cardiac rhabdomyoma associated with tuberous sclerosis, 10 males and 11 females, aged from the date of birth to 9 years at diagnosis. The mean period of follow-up was 53 months. None of the patients developed congestive heart failure. We evaluated the electrocardiographic changes during the follow-up, and their association with echocardiographic findings.Results:Of the 21 patients, 12 showed one or more abnormalities on the electrocardiogram at presentation, with five demonstrating right or left ventricular hypertrophy. In all of these five cases, the tumours were mainly located in the respective ventricular cavity. In one patient with a giant tumour expanding exteriorly, there was marked left ventricular hypertrophy on the electrocardiogram. Followup studies showed spontaneous regression of the tumours in 12 of 19 patients, with abnormalities still present in only 7 patients. A gradual disappearance of left ventricular hypertrophy as seen on the electrocardiogram was noted in the patient with marked left ventricular hypertrophy at presentation in parallel with regression of the tumour.Conclusions:The presence of cardiac rhabdomyomas in patients with tuberous sclerosis might explain the ventricular hypertrophy seen on the electrocardiogram through its electrically active tissue without ventricular pressure overload or ventricular enlargement, although pre-excitation might affect the amplitude of the QRS complex. Even in cases with large tumours, nonetheless, the electric potential might not alter the surface electrocardiogram if the direction of growth of the tumour is towards the ventricular cavity. In many cases, electrocardiographic abnormalities tend to disappear, concomitant with regression of the tumours.

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