Effects of ACE Inhibition versus Non-ACE Inhibitor Antihypertensive Treatment on Myocardial Fibrosis in Patients with Arterial Hypertension

Brilla, Christian G.; Rupp, Heinz; Maisch, Bernhard

doi:10.1007/s00059-003-2524-6

Cited by 42 publications

(34 citation statements)

References 40 publications

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“…88,89 Alternatively, kidney function is also responsible for age-associated mouse 90 and rat deaths, 91 and lower blood pressure associated with inhibiting the RAS may also reduce kidney damage. Recent data suggest that cardiac function, which is also adversely affected by angiotensin signaling, 73 may be partially responsible for mouse deaths. 89,92 AT1 angiotensin receptor inhibitors have been reported to inhibit the formation of circulating MDA-modified LDLs in human diabetic patients and the modification by MDA of lungs in rats affected with bleomycin-induced pulmonary fibrosis.…”

Section: Example #1: Renin-angiotensin Systemmentioning

confidence: 99%

Applied Healthspan Engineering

Larrick

Mendelsohn

2010

Rejuvenation Research

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According to the Homeric Hymn to Aphrodite, when Eos asked Zeus for Tithonus to be granted immortality, she forgot to ask for eternal youth. Applied Healthspan Engineering (AHE) seeks to address this problem. All organisms have a minimal level of functional reserve required to sustain life that eventually declines to a point incompatible with survival at death. AHE seeks to maintain or restore optimal functional reserve of critical tissues and organs. Tissue reserve correlates with well being. Diet, physical exercise, and currently available smallmolecule-based therapeutics may attenuate the rate of decline of specific organs or organ systems, but are unlikely to restore lost reserve. Inherent evolutionary-derived limitations in tissue homeostasis and cell maintenance necessitate the development of therapies to enhance regenerative processes and possibly replace whole organs or tissues. AHE supports the study of cell, tissue, and organ homeostatic mechanisms to derive new regenerative and tissue replacement therapies to extend the period of human health.

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Section: Example #1: Renin-angiotensin Systemmentioning

confidence: 99%

Applied Healthspan Engineering

Larrick

Mendelsohn

2010

Rejuvenation Research

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“…1 Furthermore, a recent systematic review shows that HF development remains a major problem in treated hypertensive patients. 2 It has been shown that myocardial fibrosis, a common finding in postmortem studies and endomyocardial biopsies of patients with hypertensive heart disease (HHD), 3 is associated with the increase of left ventricular (LV) chamber stiffness 4,5 and the development of clinically overt HF in these patients. 6,7 It has been proposed that the increase in LV stiffness can contribute to compromised diastolic function and elevate left-sided filling pressures (FPs) in hypertensive patients.…”

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confidence: 99%

Collagen Cross-Linking But Not Collagen Amount Associates With Elevated Filling Pressures in Hypertensive Patients With Stage C Heart Failure

et al. 2012

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Abstract-We investigated whether the quality of myocardial collagen associates with elevated left-sided filling pressures in 38 hypertensive patients with stage C chronic heart failure. Filling pressures were assessed invasively measuring pulmonary capillary wedge pressure. Left ventricular chamber stiffness constant was calculated from the deceleration time of the early mitral filling wave. The fraction of myocardial volume occupied by total collagen tissue and collagen type I fibers was assessed histomorphologically. The degree of collagen cross-linking (CCL), which determines the formation of insoluble stiff collagen, was assessed by colorimetric and enzymatic procedures. Key Words: collagen Ⅲ filling pressures Ⅲ heart failure A rterial hypertension has been long considered as one of the most common etiologic conditions predisposing to heart failure (HF).1 Furthermore, a recent systematic review shows that HF development remains a major problem in treated hypertensive patients.2 It has been shown that myocardial fibrosis, a common finding in postmortem studies and endomyocardial biopsies of patients with hypertensive heart disease (HHD), 3 is associated with the increase of left ventricular (LV) chamber stiffness 4,5 and the development of clinically overt HF in these patients. 6,7 It has been proposed that the increase in LV stiffness can contribute to compromised diastolic function and elevate left-sided filling pressures (FPs) in hypertensive patients. 8 The definition of myocardial fibrosis is based on the quantification of an excess of collagen fiber deposition, as assessed by staining techniques. However, it must be considered that collagen-dependent LV chamber stiffness is influenced not only by the amount of collagen fibers but also by their qualitative properties (ie, the degree of collagen crosslinking [CCL] among collagen fibrils that determines the insolubility, stiffness, and resistance to degradation of the resulting fibers; the relative proportions of collagen types I and III fibers; and the diameter of the collagen fibers and their spatial alignment). 9 In fact, as demonstrated in different experimental models of pressure overload, although LV chamber stiffness is affected by changes in both collagen

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“…Obgleich ACE-Hemmer im Tierexperiment in der Therapie die kardiale Fibrose völlig reversibel gestalten, können sie diese beim Menschen nur vermindern. Wie am Beispiel der arteriellen Hypertonie bioptisch gezeigt werden konnte, ist diese reverse Remodeling auch bei adäquater antihypertensiver Therapie nicht vollständig (Abbildung 13) [5]: In linksventrikulären Myokardbiopsien konnte die Kollagenvolumenfraktion zwar von 7,6% auf 5,3% vermindert werden, lag aber trotzdem noch immer erheblich über den Kontrollen mit 0,5%. Die myokardiale Steifigkeit ist zusätzlich infolge einer inadäquaten SERCA-2-Expression gesteigert, die zur gestörten Relaxation entscheidend beiträgt (Abbildung 11).…”

Section: Pathomechanismenunclassified

“…Im Hochdruckherzen ist der Vorgang komplexer. Dort sind in den Biopsien das inaktive Pro-MMP-2 vermindert und Pro-MMP-9 gesteigert [5] (Abbildung 28).…”

Section: Kollagenabbau Und Ventrikeldilatationunclassified