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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in left ventricular remodeling due to antihypertensive therapy have been demonstrated in experimental animal studies although no quantitative relationship has been shown between correction of blood pressure and regression of myocardial mass. As regards the qualitative aspects of regression, only the ACE inhibitors have been shown to prevent the development and induce regression of the excess collagen content of the myocardium submitted to chronic pressure overload. The problems posed by remodeling in clinical practice are more complex: should regression of myocardial mass itself be the therapeutic objective in the absence of a practical method of analysing the interstitial factor of hypertensive disease or should we concentrate on the satellite problems of hypertrophy which are correction of ischemia, left ventricular filling abnormalities and arrhythmias. For each of these clinical problems, the benefits attributed to changes in remodeling, though probable, are to a large degree hypothetical. The benefits offered by these drugs which reduce ventricular hypertrophy are, however, considerable.
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PMID:[Left ventricular remodeling and hypertension. Course with antihypertensive therapy]. 183 22

Local inhibition of angiotensin-converting enzyme (ACE, kininase II) produces both-attenuation of angiotensin II generation and of bradykinin degradation. To delineate the participation of bradykinin in the cardioprotective actions of ACE inhibitors, experiments were performed in rats and dogs with cardiac ischemia-reperfusion injuries. In isolated perfused working rat hearts with regional myocardial ischemia, bradykinin in concentrations as low as 1 x 10(-9) M increases coronary flow and reduces the incidence and duration of reperfusion ventricular fibrillation. In addition, enzyme activities of lactate dehydrogenase and creatine kinase as well as lactate output were decreased in the venous effluent of bradykinin-perfused hearts, which also showed improved cardiodynamic and metabolic parameters. Even concentrations of bradykinin lower than 1 x 10(-10) M, which were without influence on coronary flow, exerted comparable beneficial metabolic effects connected with reduced incidence and duration of ventricular fibrillation. Combined perfusions with threshold concentrations of bradykinin (1 x 10(-12) M) and the ACE inhibitor ramiprilat (2,58 x 10(-9) M), which were ineffective given alone, resulted in a marked cardioprotective effect. Perfusion with angiotensin II (1 x 10(-9) M) aggravated reperfusion arrhythmias and worsened myocardial metabolism. Bradykinin perfusion prevented this deterioration in a concentration-dependent manner. The bradykinin antagonist D-Arg-[Hyp2, Thi5,8, D-Phe7]-bradykinin (1 x 10(-5)) completely abolished the cardioprotective effects of bradykinin or the ACE inhibitor. However, higher concentrations of bradykinin (1 x 10(-7) M) or ramiprilat (2,58 x 10(-5) M) reversed these properties of the bradykinin antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[ACE inhibition: mechanisms of "cardioprotection" in acute myocardial ischemia]. 186 30

Acute myocardial ischemia results from an increased cardiac workload in presence of a critical coronary stenosis (demand ischemia), coronary occlusion (supply ischemia) or a combination of both. It is complicated by cardiac arrhythmias and deterioration of function of ischemic myocardium and results in an increased load and dilatation of non-ischemic myocardium. Cardiac protection in acute myocardial ischemia can be related to preservation of coronary blood flow, function of ischemic and non-ischemic myocardium or prevention of cardiac arrhythmias. In control animals and humans, ACE-inhibitors have no major effect on coronary blood flow. Myocardial ischemia raises plasma-renin-activity, angiotensin I-conversion by passage through coronary circulation, and plasma-angiotensin-II-concentrations. ACE-inhibitors and angiotensin-II-receptor blockers increase coronary blood flow during myocardial ischemia. Other mechanisms (bradykinin potentiation) may be involved. We found a potentiation of the coronary dilatory effect of the neuropeptide neurotensin (which is probably mediated by prostaglandins) by ACE-inhibitor. ACE-inhibitor may delay infarct development in animal experiments and improve function of ischemic myocardium. The importance of early dilatation of non-ischemic myocardium is unknown and it is unclear whether it may be prevented by an ACE-inhibitor as was shown for late dilatation. Studies on the effect of ACE-inhibitors in exercise-induced angina pectoris are controversial. An antiischemic and coronary dilatory effect has been shown by invasive studies in patients. A preliminary study in unstable angina pectoris was positive. Beneficial hemodynamic and antiarrhythmic effects (as well as excessive hypotension, however) have been shown in patients with acute myocardial infarction.
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PMID:[Possibilities of ACE inhibitor therapy in acute myocardial ischemia]. 186 31

Exogenous bradykinin was administered to pigs in which an experimental infarction was evoked by ischemia and reperfusion. Ischemia (45 min) was induced in a closed-chest model with a balloon catheter in the left anterior descending artery, reperfusion by deflating and removing the balloon. The pigs were treated with saline (n = 11) or bradykinin (0.1 mg/kg in 30 min) infusion (n = 10) during the last 15 min of the ischemic period and the first 15 min of reperfusion. During ischemia, heart rate increased in the saline group to 120 +/- 9% of the initial value (p less than 0.05) and in the bradykinin group to 155 +/- 13% (p less than 0.05). After reperfusion, the rate-pressure product was increased in both groups. The increase of arterial creatine kinase levels was significantly less in the bradykinin-treated group. However, the catecholamine and purine levels were increased, as was the plasma renin activity when compared with the saline group. Two weeks after the infarction, six pigs had died in each group. In three out of five surviving saline-treated pigs and one out of four surviving bradykinin-treated pigs, a sustained ventricular tachyarrhythmia was inducible after programmed electrical stimulation. In conclusion, although systemically administered bradykinin caused a temporary increase in myocardial ischemia, it did reduce the (enzymatic indices of) infarct size. Therefore, the beneficial effects, previously found for ACE-inhibitors might at least partially be related to the potentiation of endogenous bradykinin.
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PMID:Beneficial effects of bradykinin on porcine ischemic myocardium. 187 66

Eleven patients with uncomplicated mild-to-moderate hypertension (diastolic pressure 95-115 mmHg) were treated for four weeks with daily single quinapril doses of 20-40 mg. Already during the second week a significant reduction in blood pressure was observed without increase of heart rate; 27.3% of patients responded to the lower dose (diastolic blood pressure [90 mmHg], and 54.6% responded to the higher dose. Drug treatment led to reduced pressure increase in response to cold stimulation without influencing the adrenergic response both in basal conditions and after cold pressor test. The drug brought about peripheral vasodilatation as shown by increased perfusion index during Doppler ultrasound examination, and improved arterial reactivity with increased perfusion index and reduced recovery time after ischemia. The reduction of angiotensin and aldosterone plasma levels during treatment was not correlated to diminished blood pressure values, indicating that the antihypertensive effect can occur via pathways different from ACE inhibition. Tolerance was excellent as shown both by clinical and laboratory evidence.
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PMID:[Clinical-instrumental evaluation of the effects of quinapril treatment in mild-to-moderate hypertension]. 214 11

The converting enzyme not only converts angiotensin I into angiotensin II but also metabolizes bradykinin. Furthermore, the effects of ischemia on myocardial tissue damage can be modulated by converting enzyme inhibitors. It is unknown whether these effects of ACE-inhibitors are due to increased bradykinin production. In this paper we describe the effects of captopril on bradykinin production in the ischemic isolated rat heart. The reduced deleterious effects of ischemia by captopril were associated with a stimulated bradykinin production. Beneficial effects of bradykinin could be due to an improved perfusion or to an effect on cellular metabolism. Therefore, we conclude that this effect on kinins by ACE-inhibitors is of importance in modulating tissue damage during ischemia.
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PMID:The effects of bradykinin and the ischemic isolated rat heart. 216 66

From the discussion of these questions, several conclusions seem firm, whereas other issues await resolution. Patients with severe CHF should be treated with diuretics, digoxin, and an ACE inhibitor. In mild and moderate CHF, a diuretic should be combined with either digoxin or an ACE inhibitor--usually the latter. However, most of these patients would benefit from receiving all three drugs. Patients with asymptomatic left ventricular systolic dysfunction are at jeopardy for progressive deterioration. Angiotensin converting enzyme inhibitors and, possibly, direct vasodilators may prevent progression. In initiating vasodilator therapy, ACE inhibitors usually should be the agent of choice. Exceptions may be patients with ongoing ischemia in whom nitrates are an appropriate alternative and those who are poor candidates because of hypotension, renal insufficiency, or hyperkalemia.
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PMID:Should all patients with congestive heart failure and dilated cardiomyopathy be treated with vasodilators? 219 51

The protective effect of angiotensin-converting enzyme inhibitors (ACEI) on myocardial ischemia and reperfusion damage was estimated in rat hearts, both in vivo and in vitro. Enalapril 2.5 mg/kg ip pretreatment at 24 and 5 h before coronary occlusion, significantly blunted the rise of CPK (445 +/- 151 vs 649 +/- 244 mu/ml, P less than 0.05) and improved electrocardiogram (ECG) 8 h after coronary occlusion. In global ischemia and reperfusion ex vivo, enalapril improved contractility (0.9 +/- 0.2 vs 0.3 +/- 0.3 g, P less than 0.05) and coronary flow (15.6 +/- 3.3 vs 11.9 +/- 3.1 ml/min/g, P less than 0.05), shortened significantly the duration of reperfusion arrhythmia (3.1 +/- 2.7 vs 9.7 +/- 8.1 min, P less than 0.05). In Langendorffs heart, captopril remarkably preserved force of contraction (2.1 +/- 0.4 vs 1.4 +/- 0.4 g, P less than 0.01) and coronary flow (2.7 +/- 0.5 vs 3.6 +/- 0.9 ml/min/g, P less than 0.05) in segmental infarction deteriorated by angiotensin I. Captopril 10(-5) M infusion reduced the release of CPK (435 +/- 112 vs 640 +/- 123 mu/min coronary flow, P less than 0.05). This action was almost completely abolished by pretreating and infusing with indomethacin. As a positive control, prostacyclin 5 X 10(-7) M infusion further reduced the release of CPK to 330 +/- 77 mu/min. It is concluded that angiotensin-converting enzyme inhibitor can protect both myocardial ischemia and reperfusion damage in rat hearts. The mechanism of protection was ascribed to reduced production of angiotensin II by ACE inhibition and increased prostacyclin release in the myocardium.
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PMID:Protective effects of captopril and enalapril on myocardial ischemia and reperfusion damage of rat. 282 45

The myocardial scar, left behind by an infarct, makes up a potential substrate for complex ventricular arrhythmias due to the presence in such tissue of electrical inhomogeneity, altered refractoriness, and abnormal conduction properties, which facilitate the induction of reentrant arrhythmias and the release of abnormal automatic responses of the partially repolarised cells. The mechanism(s) by which complex ventricular arrhythmias is/are transformed into malignant arrhythmias has/have not yet been definitely proven. The observation that coronary revascularization - in patients with ischaemic heart disease surviving out of hospital cardiac arrest - improves the prognosis, indicates that transient ischaemic attacks might be the trigger of malignant ventricular arrhythmias in patients with prior myocardial infarction. Patients with large infarct scars (heart failure) have an increased incidence of complex ventricular arrhythmias, death, and ischaemic events. Antiarrhythmic medical intervention does not improve the prognosis in these patients. Intervention with ACE-inhibitors reduces the prevalence of complex ventricular arrhythmias, the incidence of death, and reinfarction, but not arrhythmic death, indicating that residual ischaemia might be the major risk variable in patients with heart failure. Ischaemia is one of several risk markers for transient supraventricular arrhythmias in patients recovering from an acute myocardial infarction (AMI). In addition, anti-ischaemic intervention in patients recovering from AMI suppresses residual myocardial ischaemia and thereby reduces major events.
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PMID:[Post-infarction, myocardial ischemia: clinical importance and risk factor]. 750 21

Survivors of myocardial infarction are at increased risk for another MI, congestive heart failure, ventricular arrhythmias, and sudden death. Beta blockers reduce the rate of sudden death, reinfarction, and recurrent ischemia, particularly in elderly patients. Chronic aspirin therapy has shown significant reductions in cardiovascular morbidity and mortality and is recommended for all post-MI patients who can tolerate it. ACE inhibitor therapy has shown benefit in patients with impaired LV function. Identifying post-MI patients at risk for sudden death and preventing fatal arrhythmias has proven difficult. Class I antiarrhythmics should be avoided. Amiodarone and perhaps sotalol appear promising, but large-scale trials are still ongoing.
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PMID:MI survivors: using drug therapies to protect the heart. 755 89


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