Usefulness of Serum Carboxy-Terminal Propeptide of Procollagen Type I in Assessment of the Cardioreparative Ability of Antihypertensive Treatment in Hypertensive Patients

López, Begoña; Querejeta, Ramón; Varo, Nerea; González, Arantxa; Larman, Mariano; Ubago, José L. Martínez; Díez, Javier

doi:10.1161/01.cir.104.3.286

Cited by 225 publications

(178 citation statements)

References 25 publications

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“…36 In accordance with this observation, angiotensin II receptor blockade has been shown to significantly reduce multiple markers of inflammation (C-reactive protein, TNF-a, IL-6 and monocyte chemotactic protein-1) in hypertensive patients. 37 Haemodynamic changes in atria. The excessive increase in afterload imposed by hypertension will lead to cardiac compensation with progressive thickening of the LV wall and consequent LVH.…”

Section: Atrial Fibrillationmentioning

confidence: 99%

Hypertension and cardiac arrhythmias: a review of the epidemiology, pathophysiology and clinical implications

Yiu

Tse

2008

J Hum Hypertens

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Hypertension is commonly associated with cardiac arrhythmias in patients with and without concomitant cardiovascular disease. Experimental and epidemiological studies have demonstrated potential links between hypertension and atrial and ventricular arrhythmias, although the underlying pathophysiological mechanism remains unclear. Nonetheless, the importance of hypertension as a cause of atrial and ventricular arrhythmias is not well recognized. In particular, the occurrence of left ventricular hypertrophy is a strong predictor for the development of AF, ventricular ectopy and sudden cardiac death. Recent prospective clinical trials reveal that antihypertensive therapy may delay or prevent the occurrence of cardiac arrhythmias and sudden cardiac death in patients with hypertension. Although antihypertensive agents that block the renin-angiotensin-aldosterone system appear to protect against cardiac arrhythmias, this needs to be confirmed by current ongoing clinical trials.

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Section: Atrial Fibrillationmentioning

confidence: 99%

Hypertension and cardiac arrhythmias: a review of the epidemiology, pathophysiology and clinical implications

Yiu

Tse

2008

J Hum Hypertens

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“…It has been proposed that the excess of myocardial collagen seen in hypertension is the result of both increased collagen synthesis and decreased collagen degradation. 2 Recent experimental 3,4 and clinical 5 findings suggest that the interaction of angiotensin II with its type 1 (AT 1 ) receptors plays a critical role in alterations of collagen type I metabolism and development of myocardial fibrosis in arterial hypertension.…”

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confidence: 99%

Losartan-Dependent Regression of Myocardial Fibrosis Is Associated With Reduction of Left Ventricular Chamber Stiffness in Hypertensive Patients

et al. 2002

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Background — This study was designed to investigate whether myocardial collagen content is related to myocardial stiffness in patients with essential hypertension. Methods and Results — The study was performed in 34 patients with hypertensive heart disease. Nineteen of these patients were also evaluated after 12 months of treatment with losartan. Transvenous endomyocardial biopsies of the interventricular septum were performed to quantify collagen volume fraction (CVF). Left ventricular (LV) chamber stiffness (K LV ) was determined from the deceleration time of the early mitral filling wave as measured by Doppler echocardiography. Histological analysis at baseline revealed the presence of 2 subgroups of patients: 8 with severe fibrosis and 26 with nonsevere fibrosis. Values of CVF and K LV were significantly higher in the 2 subgroups of hypertensives than in normotensives. In addition, compared with patients with nonsevere fibrosis, patients with severe fibrosis exhibited significantly increased values of CVF and K LV . After treatment, CVF and K LV decreased significantly in patients with severe fibrosis (n=7). None of these parameters changed significantly after treatment in patients with nonsevere fibrosis (n=12). CVF was directly correlated with K LV ( r =0.415, P <0.02) in all hypertensives. Conclusions — These findings show a strong association between myocardial collagen content and LV chamber stiffness in patients with essential hypertension. Our results also suggest that the ability of losartan to induce regression of severe myocardial fibrosis is associated with diminution of myocardial stiffness in hypertensive patients.

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“…Pharmacological anti-hypertensive interventions within 1 year clarified the significant difference in effects on surrogate markers observed in previous clinical studies. [38][39][40] If the number of study subjects was much more in this study, we might have observed a clear difference in the effects on markers between the two regimens. However, the desirable endpoints of clinical trials are cardiovascular and cerebrovascular events and death, and hence future clinical studies with more patients and longer observational period are required.…”

Section: Limitationsmentioning

confidence: 87%

The Effect of Losartan and Amlodipine on Left Ventricular Diastolic Function and Atherosclerosis in Japanese Patients with Mild-to-Moderate Hypertension (J-ELAN) study

Yamamoto

Ozaki²,

Takayasu

et al. 2010

Hypertens Res

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This study was a prospective, randomized, open, blinded endpoint study to assess the effects of angiotensin II type 1 receptor blocker, losartan, compared with calcium channel blocker, amlodipine, on left ventricular (LV) diastolic function and atherosclerosis of the carotid artery in Japanese patients with mild-to-moderate hypertension, LV hypertrophy, diastolic dysfunction and preserved systolic function. Fifty-seven patients were randomly assigned to losartan-or amlodipine-based treatment groups and were followed up for 18 months. Blood pressure was similarly reduced by both regimens. Losartan shortened the transmitral E-wave deceleration time, and amlodipine reduced LV mass index; however, there was no significant difference in the percent changes of these indices between the two groups. Mean carotid intima-media thickness (mean IMT) as well as plaque score significantly increased in the amlodipine-based regimen (pre: 1.05 ± 0.26 mm, follow-up: 1.23 ± 0.33 mm, P¼0.0015), but not in the losartan-based regimen (pre: 1.08 ± 0.35 mm, follow-up: 1.16 ± 0.52 mm, P¼non-significant). The percent increase in mean IMT in the amlodipine-based regimen tended to be large compared with the losartan-based regimen (amlodipine: 19.8 ± 23.7%, losartan: 6.9 ± 23.3%, P¼0.06). Under similar reduction of blood pressure, losartan is likely effective in protecting the progression of atherosclerosis of the carotid artery compared with amlodipine. Losartan may improve LV diastolic function, and amlodipine may attenuate LV hypertrophy; however, this study cannot make consecutive remarks about the superiority of either treatment regimen in the effects on cardiac function and geometry. This study has been registered at

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Usefulness of Serum Carboxy-Terminal Propeptide of Procollagen Type I in Assessment of the Cardioreparative Ability of Antihypertensive Treatment in Hypertensive Patients

Cited by 225 publications

References 25 publications

Hypertension and cardiac arrhythmias: a review of the epidemiology, pathophysiology and clinical implications

Hypertension and cardiac arrhythmias: a review of the epidemiology, pathophysiology and clinical implications

Losartan-Dependent Regression of Myocardial Fibrosis Is Associated With Reduction of Left Ventricular Chamber Stiffness in Hypertensive Patients

The Effect of Losartan and Amlodipine on Left Ventricular Diastolic Function and Atherosclerosis in Japanese Patients with Mild-to-Moderate Hypertension (J-ELAN) study

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