Diastolic disease in left ventricular hypertrophy: comparison of M mode and Doppler echocardiography for the assessment of rapid ventricular filling.

Lee, C H; Hogan, Jarred; Gibson, D G

doi:10.1136/hrt.65.4.194

Cited by 36 publications

(13 citation statements)

References 19 publications

(4 reference statements)

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“…These 2 parameters, less popular than Doppler-derived diastolic indices, have been proven more accurate and specific than Doppler parameters in discriminating between normal and abnormal diastole in patients with myocardial hypertrophy. 37 In agreement with previous reports, 1,32,38 we found an impairment of diastolic function in many lean and obese hypertensives, whereas systolic function was normal in all and similar among the 4 groups. To the best of our knowledge, this is the first study testing the hypothesis that genetic predisposition to hypertension can influence the myocardial response to insu- lin, and we think that our results support this hypothesis.…”

Section: Discussionsupporting

confidence: 82%

Insulin and Diastolic Dysfunction in Lean and Obese Hypertensives

et al. 1999

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Abstract-We investigated the influence of genetic predisposition to hypertension by studying the relation between insulin sensitivity and left ventricular (LV) mass and function in untreated lean and obese hypertensives. We selected 50 lean hypertensives with normotensive parents (negative family history of hypertension [FϪ]), 64 lean hypertensives with 1 or both parents hypertensive (positive family history of hypertension [Fϩ]), 40 obese FϪ hypertensives, and 43 obese Fϩ hypertensives. The 4 groups were comparable regarding age, gender, 24-hour blood pressure profile, and known duration of hypertension. We measured glucose, insulin, and C-peptide during fasting and during an oral glucose tolerance test; LV morphology and function were assessed by digitized M-mode echocardiography. Glucose (fasting and test) levels were normal in all and similar among the 4 groups. Insulin and C-peptide (fasting and stimulated) levels were higher in obese hypertensives than in lean hypertensives; at similar body mass index, insulin and C-peptide levels were higher in Fϩ than in FϪ groups. Compared with lean hypertensives, obese hypertensives had greater LV mass index; LV systolic function was normal in all and similar among the groups. The indices of LV diastolic function were significantly lower in Fϩ than in FϪ groups. LV mass index did not correlate with metabolic parameters; the indices of LV diastolic function were inversely correlated with insulin area during test in only the 2 Fϩ groups. In conclusion, genetic predisposition to hypertension is associated with a reduced insulin sensitivity and affects the response of the myocardium to increased insulin levels, inducing a greater impairment of diastolic function. Insulin sensitivity and genetic predisposition to hypertension seem to have no influence on LV mass. (Hypertension. 1999;34:1208-1214.)Key Words: insulin Ⅲ diastole Ⅲ hypertension, essential Ⅲ obesity Ⅲ hypertrophy E ssential hypertension and obesity are often associated, and each one, per se, can induce myocardial hypertrophy and left ventricular (LV) diastolic dysfunction. 1-5 Insulin resistance and hyperinsulinemia have been described in both hypertension and obesity. 6,7 In experimental studies, insulin has been demonstrated to exert a growth-stimulating effect on cardiomyocytes and to increase collagen production in fibroblasts 8 -12 ; therefore, clinical studies have evaluated the possible contribution of insulin resistance and hyperinsulinemia to the development of myocardial hypertrophy and diastolic dysfunction in hypertension and in obesity and have obtained conflicting results. [13][14][15][16][17][18][19][20] Recently, it has been suggested that genetic factors play an important role in the link between insulin resistance, hypertension, and obesity. In fact, a reduced insulin sensitivity has been demonstrated in lean and obese normotensives and hypertensives with hypertensive parents (positive family history of hypertension [Fϩ]) compared with offspring of normotensive parents (negative family history...

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Section: Discussionsupporting

confidence: 82%

Insulin and Diastolic Dysfunction in Lean and Obese Hypertensives

et al. 1999

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“…These indices, less used than Doppler derived parameters, have been demonstrated to be more sensitive in discriminating between normal and impaired diastolic function in the presence of myocardial hypertrophy; they are also less in¯uenced by heart rate and events occurring during isovolumic relaxation. 26 Both diastolic indices were signi®cantly lower in obese than in lean groups. Diastolic dysfunction is a key feature of hypertensive cardiomyopathy, 27,28 but in our young adults obesity appears far more relevant than recently diagnosed hypertension in affecting LV diastolic function: in obese normotensives diastolic indices were signi®cantly lower than in lean hypertensives and, at similar BMI, peak lengthening rate and peak wall thinning rate were only sligthly and not signi®-cantly lower in hypertensives compared with normotensives, despite a signi®cantly greater mass in hypertensives.…”

Section: Discussionmentioning

confidence: 99%

Obesity and left ventricular diastolic function: noninvasive study in normotensives and newly diagnosed never-treated hypertensives

et al. 2000

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OBJECTIVE: To evaluate the in¯uence of obesity, per se or associated with hypertension, on left ventricular (LV) diastolic function. PATIENTS: Thirty-two obese newly-diagnosed never-treated hypertensives; 32 obese normotensives matched for age, sex and BMI with hypertensives; 32 lean newly diagnosed never-treated hypertensives and 32 lean normotensives, matched for age, sex and 24 h blood pressure (BP) with the obese subjects. METHODS: Twenty-four-hour ambulatory blood pressure monitoring and digitized M-mode LV echocardiograms. PARAMETERS EVALUATED: Twenty-four-hour, day-time and night-time BP and heart rate, percentage nocturnal BP fall; LV end-diastolic diameter index, septal and posterior wall thickness, LV mass index, peak shortening and lengthening rate of LV diameter, peak thinning rate of LV posterior wall. RESULTS: A main effect was found for obesity on LV diameter and LV mass and for hypertension on LV mass; LV systolic function was normal in all the subjects and similar among the four groups; LV diastolic function was signi®cantly reduced in both obese groups with respect to lean ones. This difference persisted after correction of diastolic parameters for 24 h BP and heart rate, LV diameter and LV mass index and disappeared only after correction for body mass index. This latter was inversely related with diastolic parameters only in the obese groups. CONCLUSIONS: Obesity is associated with a preclinical impairment of LV diastolic function in both normotensives and hypertensives; the diastolic impairment is independent of haemodynamic factors, such as 24 h BP and heart rate, and bears no relation to LV geometry in normotensives and only little relation in hypertensives, having therefore to be ascribed to obesity itself.

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“…Moreover, they are far less influenced than Doppler indices by age and heart rate. 25 We evaluated also the more often used Doppler-derived diastolic parameters. Many studies showed that a stable and significant BP reduction is associated with regression of myocardial hypertrophy and improvement of LV diastolic function.…”

Section: Discussionmentioning

confidence: 99%

Aldosterone Antagonist Improves Diastolic Function in Essential Hypertension

et al. 2002

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Abstract-Experimental studies demonstrated that mineralocorticoid antagonists prevent or reverse myocardial fibrosis.Therefore, we tested the hypothesis that the aldosterone antagonist canrenone can improve left ventricular diastolic function in essential hypertension. Using digitized M-mode echocardiography and 24-hour blood pressure monitoring (ABPM), we realized a prospective, randomized, controlled study on 34 never-treated essential hypertensives with left ventricular diastolic dysfunction. Echocardiogram and ABPM were repeated after 6 months of effective antihypertensive treatment with ACE inhibitors and calcium antagonists (second evaluation) and then after a 6-month period with 17 patients randomly assigned to add canrenone 50 mg/d to the previous treatment (third evaluation). At the basal evaluation 32 patients had left ventricular concentric hypertrophy, and 2 patients had left ventricular concentric remodeling. All the patients had normal left ventricular systolic function. At the second evaluation blood pressure was reduced (PϽ0.0001), left ventricular mass index decreased (PϽ0.0001), and diastolic function improved (PϽ0.0001). After randomization, the canrenone and control groups had similar 24-hour blood pressure and left ventricular morpho-functional characteristics. At the third evaluation, despite unchanged blood pressure and similar decrease of left ventricular mass index, the canrenone group, compared with control group, showed a significantly greater increase in left ventricular diastolic indices. In essential hypertension, a low dose of aldosterone antagonist added to antihypertensive treatment significantly improved left ventricular diastolic function. This improvement, not accounted for by changes in blood pressure and left ventricular mass, can be therefore ascribed to a direct action of the drug on the myocardium. C ardiac remodeling in essential hypertension is characterized by myocyte hypertrophy and increased interstitial fibrosis, 1 which results from increased collagen synthesis and unchanged or decreased collagen degradation. [2][3][4] The rise in myocardial collagen content plays a major role in the development of left ventricular (LV) diastolic dysfunction by affecting both LV relaxation and stiffness. 3,[5][6][7][8] Experimental studies have demonstrated the central role of aldosterone in promoting cardiac fibrosis, probably through a direct action on the heart mediated by cardiac mineralocorticoid receptors. 9 -11 This profibrotic action, independent of blood pressure (BP) increase, 12 can be effectively opposed by aldosterone-receptor blockade. 13 In experimental studies on rats with renovascular hypertension, hyperaldosteronism, or spontaneous hypertension, the aldosterone antagonist spironolactone was able to prevent or reverse the development of myocardial fibrosis even though the drug did not normalize blood pressure and did not prevent LV hypertrophy. 14 -16 Therefore, we considered it of interest to test the hypothesis that the aldosterone antagonist canrenone can imp...

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Diastolic disease in left ventricular hypertrophy: comparison of M mode and Doppler echocardiography for the assessment of rapid ventricular filling.

Cited by 36 publications

References 19 publications

Insulin and Diastolic Dysfunction in Lean and Obese Hypertensives

Insulin and Diastolic Dysfunction in Lean and Obese Hypertensives

Obesity and left ventricular diastolic function: noninvasive study in normotensives and newly diagnosed never-treated hypertensives

Aldosterone Antagonist Improves Diastolic Function in Essential Hypertension

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