Cardioprotección: un triunfo de la biomedicina del siglo XX

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Abstract

La cardioprotección significa prevenir el daño vascular coronario y de los miocitos cardíacos, lo cual se obtiene por mecanismos internos del organismo y a través de diversos fármacos. Esto involucra la vasodilatación, inhibición de la generación de radicales libres de oxígeno, aumento de los niveles de ATP tisular y reducción del daño microvascular. Se revisan los mecanismos de la cardioprotección endógena, metabólica y farmacológica y se destaca la función de los betabloqueadores, anticálcicos, inhibidores de la enzima de conversión de angiotensina y por último la trimetazidina como antiisquémico celular.

Translated abstract

Cardioprotection means prevention of vascular coronary damage and of cardiac cyocites, which is achieved by internal mechanism of the body and through various pharmaceuticals. This involves vasodilation, inhibition of oxygen free radical generation, incresase of tissue ATP and reduction of microvascular damage. The mechanisms of endogenous, metabolic and phatmacological cardioprotection are reviewed, and also the function of betablokers, calcium channel blockers, angiotensin-converting enzime inhibitors, and the use of trimetazidine as anti-cell ischemia are underlined.

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Most cited references 16

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Therapeutic value of a cardioprotective agent in patients with severe ischaemic cardiomyopathy.

C Lascoux-Combe, L Brottier, J-M Bonnet … (1990)

Trimetazidine (TMZ) has been shown to have anti-ischaemic properties improving exercise tolerance without haemodynamic effects. A 6-month double-blind placebo-controlled study was carried out in 20 patients, mean age 59 +/- 6 years, to examine the benefit of adding 60 mg of TMZ vs placebo to the classical therapy, excluding those previously treated with calcium-antagonists, conversion enzyme inhibitors, vasodilators and antiplatelet agents. All patients had severe ischaemic cardiomyopathy, confirmed by coronary angiography; six were in NYHA class IV; 14 in NYHA class III; four had mild recurrent angina pectoris. assessment included clinical and biological evaluation, electrocardiography (ECG), 24-h ECG monitoring, cardiac volume evaluation with chest X-ray, left ventricular fractional shortening by echocardiography, left ventricular ejection fraction by radionuclide angiography. Baseline characteristics were similar in placebo (11 patients) and TMZ (nine patients) groups. Eighteen patients (nine in each group) were followed up for 6 months. In eight patients of the placebo group, treatment had to be modified (addition of calcium antagonists: four patients, conversion enzyme inhibitors: two patients; digitalics: one patient; diuretics: one patient). In the TMZ group, digitalic therapy was withdrawn in one patient and added in one patient (P less than 0.01). At 6 months, all TMZ group patients were free from angina; dyspnoea was improved in all TMZ patients and in only one placebo patient (P less than 0.001). Ejection fraction, increased by 9.3% in the TMZ group and decreased by 15.6% in the placebo group (P less than 0.018), CV decreased by 7% with TMZ, increased by 4% with placebo. (P = 0.034).(ABSTRACT TRUNCATED AT 250 WORDS)

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Determinants of a protective effect of glucose and insulin on the ischemic myocardium. Effects on contractile function, diastolic compliance, metabolism, and ultrastructure during ischemia and reperfusion.

C Apstein, C Haudenschild, F Gravino (1983)

The efficacy of hyperglycemia and insulin therapy for reducing ischemic myocardial injury is controversial and unproven. Accordingly, factors that might influence the effects of hyperglycemia and insulin were studied in isolated perfused rabbit hearts at two degrees of global ischemia, either "severe" or "moderate." During the ischemic period, different groups (n = 15-28/group) received either 100 mg/100 ml glucose-no insulin (control group), 500 mg/100 ml glucose + 100 mU/ml insulin (G + I), or 100 mg/100 ml glucose + 400 mg/100 ml mannitol (osmotic control). During moderate ischemia, effective washout of myocardial lactate was maintained, and hyperglycemia and insulin doubled the glycolytic flux, completely prevented contracture during ischemia, decreased contracture during reperfusion, increased recovery of postischemic contractile function, decreased ultrastructural damage, and increased high energy phosphate levels. Hyperglycemia and insulin increased glycolytic flux only after 30 minutes of ischemia had elapsed, suggesting that endogenous glycogen provided adequate glycolytic substrate prior to this time. The mannitol-glucose substrate had no beneficial effects, indicating that the hyperglycemia and insulin substrate had a metabolic rather than an osmotic mechanism of action. In contrast, during severe ischemia, tissue lactate washout was ineffective; the hyperglycemia and insulin substrate increased glycolytic flux by only 15% and produced no persistent beneficial effects. These results suggest that hyperglycemia and insulin therapy is beneficial to the ischemic myocardium when two conditions are met. First, the degree of myocardial perfusion, although in the ischemic range, must be adequate to prevent the accumulation of high tissue levels of lactate which inhibit glycolysis and prevent any glycolytic stimulation by hyperglycemia and insulin. Second, the ischemic myocardium must be "glucose dependent" for glycolytic substrate; in our studies this occurred after 30-45 minutes of sustained ischemia, probably because myocardial glycogen stores became depleted.

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Subcellular basis of myocardial stunning and hibernation

GR HEYNDRICKX, GR Heyndrickx (1996)

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Author and article information

Contributors

Iliana Cabrera Rojo: Role: ND

Journal

Journal ID (publisher): ibi

Title: Revista Cubana de Investigaciones Biomédicas

Abbreviated Title: Rev Cubana Invest Bioméd

Publisher: ECIMED (Ciudad de la Habana )

ISSN: 1561-3011

Publication date (Print): August 1999

Volume: 18

Issue: 2

Pages: 146-150

Affiliations

[1 ] Hospital Universitario General Calixto García Cuba

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Publisher ID: S0864-03001999000200012

SO-VID: 873ebcac-c449-483c-9a52-a3fd77270927

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http://creativecommons.org/licenses/by/4.0/

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SciELO Cuba

Self URI (journal page): http://scielo.sld.cu/scielo.php?script=sci_serial&pid=0864-0300&lng=en

Cardioprotección: un triunfo de la biomedicina del siglo XX

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Most cited references 16

Therapeutic value of a cardioprotective agent in patients with severe ischaemic cardiomyopathy.

Determinants of a protective effect of glucose and insulin on the ischemic myocardium. Effects on contractile function, diastolic compliance, metabolism, and ultrastructure during ischemia and reperfusion.

Subcellular basis of myocardial stunning and hibernation

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