Trandolapril Decreases Prevalence of Ventricular Ectopic Activity in Middle-Aged SHR

Chevalier, Brigitte; Heudes, Didier; Heymes, Christophe; Basset, Alexandra; Dakhli, Thierry; Bansard, Y.; Jouquey, Simone; Hamon, Gilles; Bruneval, Patrick; Swynghedauw, Bernard; Carré, François

doi:10.1161/01.cir.92.7.1947

Cited by 41 publications

(20 citation statements)

References 28 publications

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“…This effect of ACE inhibitors seems not to be restricted to aging. In fact, a significant reduction in the incidence of ectopic beats has been observed in experimental (33,34) and clinical (35) arterial hypertension, acute myocardial infarction (36) and congestive heart failure (37) after chronic ACE inhibition. There are a number of hypotheses to explain this antiarrhythmic effect.…”

Section: Discussionmentioning

confidence: 99%

Chronic converting enzyme inhibition normalizes QT interval in aging rats

Silva

Neto

Salgado

et al. 2002

Braz J Med Biol Res

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The aim of the present study was to investigate the effects of converting enzyme inhibition by captopril on ECG parameters in aged rats. Four-month-old male rats received captopril dissolved in tap water (0.5 mg/l) or tap water for 2 or 20 months. At the end of treatment, under anesthesia, RR and PR interval, P wave and QRS duration, QT and corrected QT interval were measured in all animals. On the following day, chronic ECG (lead II) recordings were performed to quantify supraventricular (SVPB) or ventricular premature beats (VPB). After sacrifice, the hearts were removed and weighed. RR interval was similar in young and untreated aged rats, but significantly larger in aged rats treated with captopril. P wave and QRS length did not differ among groups. PR interval was significantly larger in old than in young rats and was not affected by captopril. Corrected QT interval was larger in aged than in young rats (117 ± 4 vs 64 ± 6 ms, P<0.05) and was reduced by captopril (71 ± 6 ms, P<0.05). VPB were absent in young rats and highly frequent in untreated old animals (8.4 ± 3.0/30 min). Captopril significantly reduced VPB in old rats (0.3 ± 0.1/30 min, P<0.05). The cardiac hypertrophy found in untreated aged rats was prevented by captopril (3.44 ± 0.14 vs 3.07 ± 0.10 mg/g, P<0.05). The beneficial effects of angiotensin converting enzyme inhibition on the rat heart during the aging process are remarkable.

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Section: Discussionmentioning

confidence: 99%

Chronic converting enzyme inhibition normalizes QT interval in aging rats

Silva

Neto

Salgado

et al. 2002

Braz J Med Biol Res

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“…Left ventricular dimensions were determined with an image analyzer (Nachet NS 15000, Nachet-Vision, les Ulis, France; ref. 26 …”

Section: Methodsmentioning

confidence: 99%

Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice

Meneton

Bloch-Faure

Hagege

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

152

148

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Tissue kallikrein is a serine protease thought to be involved in the generation of bioactive peptide kinins in many organs like the kidneys, colon, salivary glands, pancreas, and blood vessels. Low renal synthesis and urinary excretion of tissue kallikrein have been repeatedly linked to hypertension in animals and humans, but the exact role of the protease in cardiovascular function has not been established largely because of the lack of specific inhibitors. This study demonstrates that mice lacking tissue kallikrein are unable to generate significant levels of kinins in most tissues and develop cardiovascular abnormalities early in adulthood despite normal blood pressure. The heart exhibits septum and posterior wall thinning and a tendency to dilatation resulting in reduced left ventricular mass. Cardiac function estimated in vivo and in vitro is decreased both under basal conditions and in response to ␤-adrenergic stimulation. Furthermore, flow-induced vasodilatation is impaired in isolated perfused carotid arteries, which express, like the heart, low levels of the protease. These data show that tissue kallikrein is the main kinin-generating enzyme in vivo and that a functional kallikrein-kinin system is necessary for normal cardiac and arterial function in the mouse. They suggest that the kallikrein-kinin system could be involved in the development or progression of cardiovascular diseases.

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“…A daily dose of 1 mg/kg per day trandolapril has previously demonstrated its efficiency in reducing cardiac hypertrophy in SHR. 5,10 …”

Section: Animal Model and Experimental Protocolmentioning

confidence: 99%

“…5 Briefly, with the rats anesthetized (Na ϩ pentobarbital, 25 mg/kg IP), an emitter (ETA-F20, Data Sciences) was subcutaneously implanted in the abdomen. Two leads were placed in the direction of the forelimbs to obtain a derivation similar to lead II in humans.…”

Section: Ecg Monitoring and Measurement Of Heart Rate Variabilitymentioning

confidence: 99%

Converting Enzyme Inhibition Normalizes QT Interval in Spontaneously Hypertensive Rats

et al. 2000

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Abstract-We quantified the repolarization time (so-called QT interval) in a rat, an animal species that does not show a well-characterized T wave on surface ECG. We used spontaneously hypertensive rats (SHR) and converting enzyme inhibition to demonstrate a reversible increase in QT interval in pressure-overloaded hearts in the absence of ischemia. An implanted telemetry system recording ECG data in freely moving rats was used to automatically calculate the RR interval. The QT duration was manually determined by use of a calibrated gauge, and a time-frequency domain analysis was used to evaluate heart rate variability. Left ventricular mass was sequentially assessed by echocardiography. Before treatment, 12-month-old SHR had higher left ventricular mass, QT and RR intervals, and unchanged heart rate variability compared with age-matched Wistar rats. A 2-month converting enzyme inhibition treatment with trandolapril reduces systolic blood pressure, left ventricular mass, and QT interval. The RR interval and heart rate variability remains unchanged. There is a positive correlation between the QT interval and left ventricular mass. The SHR is suitable for longitudinal studies on the QT interval. Thus, the detection of the QT interval reflects the phenotypic changes that occur during mechanical overload and, on the basis of these criteria, allows an in vivo determination of the adaptational process. Key Words: hypertrophy Ⅲ hypertension, arterial Ⅲ electrocardiography Ⅲ converting enzyme inhibition Ⅲ QT interval S everal ECG indexes have been proposed for identifying patients at risk of sudden death, including an increased QT-interval dispersion. [1][2][3] Clinical trials had demonstrated that this index is specifically altered in chronic cardiac hypertrophy and/or during myocardial ischemia and is reversible under therapy. Nevertheless, the meaning of the QTinterval dispersion is a complex issue that includes at least 2 different phenomena, namely, a lengthening of the average duration of the action potential (AP) and myocardial heterogeneity; indeed, in clinical conditions, the QT interval is both prolonged and dispersed, because hypertensive cardiopathy usually associates cardiac hypertrophy with myocardial fibrosis. 4 -7 There is a need for models of pure mechanical overload without any ischemia, a condition that is nearly impossible to observe in clinical situations, and experimental animal models would help to resolve this issue. Among different animal species, the rat may be an ideal model because it never suffers from atherosclerosis. In addition, there exists a welldocumented rat strain, the spontaneously hypertensive rat (SHR), which complies with the above criteria and has been extensively used for pharmacological research and particularly in experimental testing of most of the available antihypertensive drugs.The QT interval represents repolarization time. It is not easy to measure in humans, despite a well-characterized T wave. In rats, the situation is still more difficult because the T wave is not c...

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Trandolapril Decreases Prevalence of Ventricular Ectopic Activity in Middle-Aged SHR

Cited by 41 publications

References 28 publications

Chronic converting enzyme inhibition normalizes QT interval in aging rats

Chronic converting enzyme inhibition normalizes QT interval in aging rats

Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice

Converting Enzyme Inhibition Normalizes QT Interval in Spontaneously Hypertensive Rats

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