The Heart in Hypertension

Fröhlich, Edward D.; Apstein, Carl S.; Chobanian, Aram V.; Devereux, Richard B.; Dustan, Harriet P.; Dzau, Victor J.; Fauad-Tarazi, Fetnat; Horan, Michael J.; Marcus, Melvin L.; Massie, Barry M.; Pfeffer, Marc A.; Ré, Richard N.; Roccella, Edward J.; Savage, Daniel D.; Shub, Clarence

doi:10.1056/nejm199210013271406

Cited by 653 publications

(274 citation statements)

References 150 publications

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“…This is especially true when repolarization abnormalities are present.31 LVH also is associated with increased risk for arrhythmias32-36 and sudden death. 8,20,37 This study also provides evidence for an association of increased voltage and repolarization abnormalities on the baseline ECG with higher blood pressures. Subjects in whom serial ECGs revealed improvement in voltage or repolarization also tended to have a concomitant decline in blood pressure.…”

Section: Additional Analysessupporting

confidence: 58%

Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy.

et al. 1994

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Section: Additional Analysessupporting

confidence: 58%

Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy.

et al. 1994

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“…30 Epidemiological and basic studies support the notion that Na ϩ is an independent factor for the development of myocardial hypertrophy. 31,32 Frohlich and colleagues 33 reported that a high Na ϩ diet increased not only cardiac enlargement in SHR but also cardiac mass in normotensive rats without detectable change of arterial pressure.…”

Section: Baseline and Cariporide-induced Changes In Sbp Lvw Lvw/bwmentioning

confidence: 99%

Regression of Hypertensive Myocardial Fibrosis by Na ⁺ /H ⁺ Exchange Inhibition

et al. 2003

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Abstract-We have recently reported that the inhibition of the Na ϩ /H ϩ exchanger (NHE) during 1 month in spontaneously hypertensive rats (SHR) is followed by regression of cardiomyocyte hypertrophy but not of myocardial fibrosis. The aim of this study was to evaluate whether a treatment of longer duration could reduce myocardial fibrosis and stiffness. SHR received 3.0 mg/kg per day of the specific NHE-1 inhibitor cariporide; the effect on cardiomyocyte cross-sectional area, myocardial collagen volume fraction, collagen synthesis, and myocardial stiffness (length-tension relation in left papillary muscles) was evaluated at several time points (after 1, 2, or 3 months). A slight decrease of Ϸ5 mm Hg in systolic blood pressure was observed after 1 month of treatment with no further changes. After 2 and 3 months of treatment, the size of cardiomyocytes remained within normal values and myocardial fibrosis progressively decreased to normal level. Accordingly, myocardial stiffness and the serum levels of the carboxyterminal propeptide of procollagen type I, a marker of collagen type I synthesis, were normalized after 3 months. Left ventricular weight decreased from 910Ϯ43 (in untreated SHR) to 781Ϯ21 mg (treated SHR) after 3 months of treatment. No difference in body weight between treated and untreated SHR was observed after this period of treatment. The present data allow us to conclude that in the SHR the administration of an NHE-1 inhibitor for 2 or 3 months leads to the normalization of collagen type I synthesis, myocardial collagen volume fraction, and stiffness. Key Words: fibrosis Ⅲ myocardium Ⅲ extracellular matrix Ⅲ signal transduction F ibrous tissue accumulation is a feature of the structural remodeling of the myocardium seen in hypertensive heart disease. 1 An exaggerated accumulation of collagen type I and type III occurs in the hypertrophied myocardium and also in the nonhypertrophied right ventricle and in the atria of animals and humans with arterial hypertension. This collagen accumulation has adverse effects. It results in the development of increased myocardial stiffness that leads to diastolic dysfunction and ultimately to the development of systolic dysfunction.Recently, a new therapeutic strategy against hypertrophy has emerged from the use of Na ϩ /H ϩ exchanger (NHE) inhibitors. [2][3][4][5] The inhibition of NHE-1 reduces the hypertrophy of the surviving myocytes after myocardial infarction 3 and of the hearts of spontaneously hypertensive rats (SHR) 2 and mice overexpressing ␤ 1 -adrenergic receptors. 4 Taken together, these findings seem to indicate a key role of NHE activity in the development of myocardial hypertrophy. Even though our recent study showed that neither myocardial fibrosis nor stiffness was normalized in the SHR after 1 month of cariporide treatment, 2 the regression of fibrosis was observed after 6 months of NHE inhibition in another model of cardiac hypertrophy, the transgenic mice overexpressing ␤ 1 -adrenergic receptors. 4 Considering that the regression of myocyte hyp...

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“…21,22 However, a dissociation between LVH and blood pressure levels has been reported in an experimental study in New Zealand genetically hypertensive rats. 23 On the other hand, HLAs that are expressed on the surface of myocardial cells have been implicated in the pathophysiology of dilated cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

HLA phenotypes as promoters of cardiovascular remodelling in subjects with arterial hypertension

et al. 2003

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The objective of this study was to investigate the association between human leukocyte antigens (HLA) phenotypes and cardiovascular remodelling, as expressed by left ventricular mass (LVM) and carotid intima-media thickness (IMT), in hypertensives. We examined 153 subjects with arterial hypertension and 61 normotensive controls living in the greater Athens area. The population was classified into three groups and specifically group I (normotensives), group II with Grade 1 hypertension and group III with Grade 2 or 3 hypertension. HLA class I and class II antigens were studied by microlymphocytotoxic technique. Carotid IMT and LVM were determined by ultrasonography. The prevalence of HLA DQ7 in the hypertensive cohort was 27.4% that was significantly smaller than the 52.5% among the controls (P ¼ 0.002). The HLA DR11 was found in 24.0% of the hypertensives and in 52.5% of the controls (Po0.001). Group III hypertensives with HLA DR11 exhibited significantly higher LVM/h in comparison to the hypertensives without this HLA (199.0 7 28.8 vs 171.2+44.1g/m, P ¼ 0.009). This association was not present in groups I and II. Similarly, group III hypertensives with HLA DQ7 were characterized by higher IMT in comparison to those without this HLA (0.94 7 0.19 vs 0.83 7 0.23 mm, P ¼ 0.048). HLA DR17 was associated with higher IMT in both groups II and III (1.00 7 0.19 vs 0.82 7 0.19 mm, P ¼ 0.046 and 1.01 7 0.23 vs 0.84 7 0.22 mm, P ¼ 0.049, respectively) but not in group I. In conclusion, certain HLA phenotypes may be related to the levels of arterial blood pressure. Moreover, it seems that these HLA phenotypes may identify subjects with arterial hypertension that are more prone to develop cardiovascular hypertrophy.

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The Heart in Hypertension

Cited by 653 publications

References 150 publications

Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy.

Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy.

Regression of Hypertensive Myocardial Fibrosis by Na ⁺ /H ⁺ Exchange Inhibition

HLA phenotypes as promoters of cardiovascular remodelling in subjects with arterial hypertension

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The Heart in Hypertension

Cited by 653 publications

References 150 publications

Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy.

Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy.

Regression of Hypertensive Myocardial Fibrosis by Na + /H + Exchange Inhibition

HLA phenotypes as promoters of cardiovascular remodelling in subjects with arterial hypertension

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Regression of Hypertensive Myocardial Fibrosis by Na ⁺ /H ⁺ Exchange Inhibition