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PubMed2000

Asymptomatic left ventricular dysfunction in the community.

The syndrome of chronic heart failure (CHF) is usually attributable to left ventricular dysfunction (LVD), which is most commonly systolic in nature. Many patients who go on to develop heart failure pass through a phase in which they have significant systolic dysfunction but lack clinical symptoms and signs: so-called asymptomatic LVD (ALVD). Treatment of this asymptomatic phase with angiotensin-converting enzyme inhibitors can delay the progression to CHF and ameliorate its substantial morbidity and mortality. This article reviews the epidemiology of ALVD. ALVD is at least as prevalent as CHF, is mainly caused by ischemic heart disease, significantly impairs effort capacity, reduces quality of life, and is associated with a substantial mortality rate. As such, it would appear to satisfy many of the criteria required to screen for a disease. The natriuretic peptide hormones (atrial natriuretic peptide and brain natriuretic peptide ) are elevated in subjects with ALVD. BNP, in particular, has acceptable accuracy to detect LVD in the general population. In particular, it has a high negative predictive value meaning a low concentration makes the presence of significant LVD highly unlikely. As such it has the potential to be a cost-effective means of filtering subjects suspected of having LVD and allowing more appropriate use of tertiary referrals for specialist assessment and detailed echocardiography.

Disease Progression↗

PubMed1986

Atrial natriuretic peptide in chronic heart failure in the rat: a correlation with ventricular dysfunction.

To assess the relation between atrial natriuretic peptide and ventricular dysfunction, we simultaneously measured both atrial and plasma immunoreactive atrial natriuretic peptide concentrations in rats 4 weeks after myocardial infarction induced by left coronary artery ligation. When compared to controls (n = 39), rats with infarction (n = 16) had markedly elevated plasma immunoreactive atrial natriuretic peptide concentrations (1205.8 +/- 180.9 vs. 126.7 +/- 8.9 pg/ml, p less than 0.001) and reduced immunoreactive atrial natriuretic peptide concentrations in right and left atria (31.4 +/- 4.6 vs. 61.2 +/- 3.2 ng/mg, p less than 0.001; 14.9 +/- 2.2 vs. 32.7 +/- 2.4 ng/mg, p less than 0.001, respectively). Right ventricular weight increased in proportion to infarct size, and both were correlated with plasma immunoreactive atrial natriuretic peptide levels (r = 0.825, p less than 0.001 and r = 0.816, p less than 0.001, respectively). Right atrial immunoreactive atrial natriuretic peptide content was significantly higher than left in both controls and rats with infarction. Both right and left atrial immunoreactive atrial natriuretic peptide concentrations were negatively correlated with both right ventricular weight as well as plasma immunoreactive atrial natriuretic peptide concentrations (right atrium: r = -0.816, p less than 0.001, r = -0.708, p less than 0.01; left atrium: r = -0.687, p less than 0.01, r = -0.644, p less than 0.01, respectively). These results suggest that chronic stimulation of atrial natriuretic peptide release from both atria is associated with increased turnover and depleted stores of atrial natriuretic peptide in atria in proportion to the severity of heart failure. It also suggests that plasma atrial natriuretic peptide levels may be used as a reliable index of cardiac decompensation in chronic heart failure.

Animals↗

PubMed1994

Role of thallium-201 and PET imaging in evaluation of myocardial viability and management of patients with coronary artery disease and left ventricular dysfunction.

The reported mortality of patients with coronary artery disease (CAD) and congestive heart failure is high but variable. In the clinical management of these patients, the available treatment choices are medical therapy, cardiac transplantation and myocardial revascularization. Myocardial revascularization has become an attractive alternative in the management of patients with CAD and poor left ventricular function because medical therapy is associated with a high mortality and cardiac transplantation is expensive and not practical due to shortage of donor hearts. Myocardial revascularization, however, should be recommended in those patients in whom the procedure is very likely to reverse regional and global left ventricular dysfunction and to improve heart failure symptoms and survival. Thallium-201 rest-redistribution myocardial scintigraphy and PET imaging of myocardial perfusion and 18F-fluoro-deoxyglucose metabolism have been extensively evaluated for the assessment of myocardial viability and for prediction of recovery of regional left ventricular dysfunction following myocardial revascularization; with positive and negative predictive accuracies of 72% and 70% for 201Tl rest-redistribution imaging and 83% and 84% for perfusion-metabolism PET imaging. Both modalities also are predictive of improvement in left ventricular ejection fraction after myocardial revascularization. Patients with congestive heart failure who demonstrate the PET pattern of mismatch are more likely to improve their heart failure symptoms following revascularization than those without the mismatch pattern. Furthermore, the PET pattern of mismatch identifies a subgroup of patients who are at very high risk for cardiac death on medical therapy. Survival of these patients can be significantly improved by myocardial revascularization.

Coronary Artery Bypass↗

PubMed1990

Improvement of left ventricular contractility and relaxation with the beta 1-adrenergic receptor partial agonist xamoterol at rest and during exercise in patients with postinfarction left ventricular dysfunction. A placebo-controlled randomized trial.

A new cardioselective beta 1-adrenergic receptor agonist xamoterol (Corwin) has been developed for the treatment of heart failure. To study the acute hemodynamic effects of xamoterol, 24 patients, 39-70 years old, with mild-to-moderate postinfarction left ventricular dysfunction entered a double-blind, between-patient comparison of a single 5-minute intravenous infusion of xamoterol (0.2 mg/kg) and placebo. The acute hemodynamic effects of xamoterol were measured at rest and during two multistaged symptom-limited supine bicycle exercise tests (Ex-T), a control Ex-T followed by an Ex-T with either xamoterol or placebo. Compared with placebo, xamoterol significantly increased left ventricular contractility (Vmax and positive [+] dP/dt) and enhanced relaxation (dP/dt- and time constant relaxation) at rest and at the 25% and 50% levels of maximum exercise. The heart rate, the frequency and time to onset of anginal symptoms, the magnitude of exercise-induced ST segment depression, the left ventricular end-diastolic and peak systolic pressures, the mean pulmonary artery pressures, the cardiac index, the left ventricular stroke-work index, and the epinephrine and norepinephrine plasma levels at rest and during exercise did not differ significantly between placebo xamoterol groups. Thus, xamoterol can be a useful addition for the treatment of left ventricular dysfunction because of long-term ischemic heart disease.

Adrenergic beta-Agonists↗

PubMed2004

Long-term outcome of isolated coronary artery bypass surgery in patients with severe left ventricular dysfunction.

BACKGROUND: Coronary artery bypass grafting (CABG) is indicated in patients with coronary artery disease and impaired ventricular function. However, earlier studies have suggested that prognosis of patients with severe left ventricular dysfunction is extremely poor. We used the APPROACH registry to derive contemporary estimates of prognosis associated with CABG for this high-risk patient population. METHODS AND RESULTS: The study group consisted of 7841 patients who had isolated CABG in the province of Alberta, Canada between 1996 and 2001. Patients with markedly reduced left ventricular function (ejection fraction [EF] <30%, Lo EF, n =430) were compared with those with moderate reduction in ventricular function (EF 30% to 50%, Med EF, n =2581) and those with normal left ventricular function (EF >50%, normal [Nl] EF, n=4830). The operative mortality was higher in the patient group with Lo EF (4.6%) compared with Med EF and Nl EF groups (3.4% and 1.9%, respectively, P<0.001). At 5 years, survival was 77.7% for Lo EF patients compared with 85.5% and 91.2% for Med EF and Nl EF patients, respectively (P<0.001). After controlling for other independent variables, the adjusted hazard ratio for death was 1.98 (95% CI, 1.49 to 2.62) for Lo EF relative to Nl EF. The mortality rate at 1 year was significantly lower for Lo EF patients who underwent CABG than it was for nonrevascularized Lo EF patients (risk-adjusted odds ratio, 0.36; 95% CI, 0.24 to 0.55). CONCLUSIONS: In the modern era of cardiac surgery, CABG can be performed in Lo EF cases with an acceptable perioperative mortality risk. Our estimate of 5-year survival in this high-risk group is better than previously reported in the literature from earlier periods.

Aged↗

PubMed1999

Does acute volume overloading in the setting of left ventricular dysfunction and pulmonary hypertension affect the defibrillation threshold?

The impact of acute volume overload hemodynamics on the DFT with concurrent moderate left ventricular systolic dysfunction is unknown. Ten mongrel dogs (17.2 kg), using a crossover study design, each had baseline (study 1) hemodynamic, echocardiographic, and DFT measurements. These measurements were repeated after left ventricular dysfunction was induced using a norepinephrine (5 micrograms/kg per min) infusion (study 2). Hemodynamic and DFT parameters were obtained simulating acute heart failure by volume overload with an 0.9% normal saline infusion to an associated mean pulmonary capillary wedge pressure of > 19 mmHg (study 3). Numerous significant echocardiographic and hemodynamic parameters were noted when the animals from studies 1 and 2, 2 and 3, and 1 and 3 were compared. A significant difference in the DFT was observed only when study animals 1 and 3 were compared (P < 0.02). None of the dogs were hypoxemic at the time of the acute heart failure DFT. The mechanism of this finding remains unknown. This data would suggest that acute volume overload with associated left ventricular dysfunction does adversely affect the DFT in a canine model.

Acute Disease↗

PubMedDate not supplied

[Usefulness of Levosimendan in patients with ventricular dysfunction before surgery].

UNLABELLED: The purpose of this work was to observe the hemodynamic stability on the first 24 hours in 4 patients with ventricular dysfunction (Ejected Fraction < 40 %), considered of high surgical risk, in which 24 at 48 hr before the surgery received an infusion of Levosimendan for 24 hours. This 4 patients was male, with age 55.5+/-7.9 years old, a left ventricle ejection of fraction (LVEF) of 31+/-5.47%; Two of them was underwent to valve replacement, another one to coronary artery bypass graft and the last one patient underwent combined procedure (coronary artery bypass graft surgery and valve replacement). The behavior of the hemodynamic parameters was stable, without necessity of uses high dose of the inotropios and classic vasopresores in the postoperative. CONCLUSION: the Levosimendan could be an inotropic of great application in this group of patient due to its novel action mechanism and to its sustained hemodynamic effects after having finished its infusion.

Cardiac Surgical Procedures↗

PubMed2005

Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms.

Tako-tsubo-like left ventricular dysfunction phenomenon (TTP) has primarily been described in Japan and is characterized by transient left ventricular apical ballooning in the absence of coronary artery disease, associated with chest symptoms, electrocardiographic changes and minimal cardiac enzymes release. Aim of the present review is to summarize the current knowledge about TTP. TTP has been described predominantly in females. TTP occurs also outside Japan. Clinical symptoms comprise anginal chest pain, dyspnea and syncope. TTP occurs frequently after acute emotional or physical stress. Electrocardiographic ST- elevations may be present only for several hours. Then, normalization of the ST-segment occurs, followed by negative T waves, which persist for months. Arterial hypertension in TTP is found in up to 76%, hyperlipidaemia in up to 57%, diabetes mellitus in up to 12% and smoking in up to 18% of the patients. Several pathomechanisms have been proposed: myocardial stunning due to increased catecholamine levels, coronary vasospasm, atherosclerotic plaques rupture, myocarditis, catecholamine-induced hyperkinesis of the basal left ventricular segments and genetic. Patients with TTP should be monitored like patients with myocardial infarction. Care should be taken in the application of catecholamines and nitrates. Betablockers should be given in the acute and chronic phase, and possibly indefinitely to prevent recurrences. The prognosis of TTP is assumed to be good, but in the acute phase there are deaths due to multisystem organ failure, cardiogenic shock, ventricular fibrillation and ventricular rupture. The long term prognosis of TTP patients is largely unknown.

Humans↗

PubMed1987

[Mid-term outcome of acute right ventricular dysfunction in biventricular myocardial infarction. Hemodynamic and cineangiographic studies].

This study was designed to evaluate the mid-term outcome of the right ventricular (RV) dysfunction which characterizes infarction of both ventricles in the acute phase. Thirteen patients hospitalized for inaugural posterior or infero-posterior infarction extending to the right ventricle (haemodynamic and cineangiographic diagnosis) were explored in the acute phase and 4 months later by right heart catheterization and selective cineangiography of the right ventricle in a 30 degrees RAO projection. The results were compared with those obtained in a control group. Haemodynamically, the RV filling pressures (p less than 0.001) and the indices of RV dysfunction--i.e. RV end-diastolic pressure/RV systolic pressure ratio (p less than 0.001) and right atrial pressure/pulmonary wedge pressure ratio (p less than 0.02)--were significantly decreased between the acute and chronic phases, but they remained pathological compared with those measured in the control group. Angiographically, the right ventricular dysfunction in the acute phase was reflected in an increase of the RV end-systolic volume (p less than 0.02) and a decrease of the RV ejection fraction (p less than 0.01), whereas diastolic cavitary dilatation was inconstant, with mean values of RV end-diastolic volume close to those found in the control group. The systolic dysfunction persisted, unchanged, during the chronic phase. Segmental kinetics of the inferior wall was much reduced in the acute phase (p less than 0.001), this hypokinesia partially regressing in the chronic phase; but in fact there were wide individual variations, and some patients even recovered an almost normal contractility. Tricuspid valve regurgitation was frequent (6/13 cases) in the acute phase and regressed in 2 out of 3 cases in the chronic phase; its presence introduced a degree of bias in the measurement of RV end-systolic volume and RV ejection fraction, with a tendency to underestimate the severity of diastolic dysfunction. To summarize, right ventricular dysfunction was constant but often modest in the acute phase and remained relatively stable at mid-term, whereas segmental kinetics of the inferior wall improved, sometimes dramatically.

Adult↗

PubMed1993

Activation of neurohumoral systems in postinfarction left ventricular dysfunction.

OBJECTIVES: This study was conducted to evaluate the degree of neurohumoral activation around the time of hospital discharge after myocardial infarction. BACKGROUND: Because pharmacologic interventions that block the effects of neurohumoral activation improve the prognosis after infarction, we hypothesized that widespread neurohumoral activation persists in some patients until at least the time of hospital discharge and that the determinants of activation vary from one system to another. METHODS: Five hundred nineteen patients in the Survival and Ventricular Enlargement Study (SAVE) had plasma neurohormones measured before randomization at a mean of 12 days after infarction. All patients had left ventricular dysfunction (left ventricular ejection fraction < or = 40%) but no overt heart failure. RESULTS: Although all neurohormones except epinephrine were increased compared with values in age-matched control subjects, plasma norepinephrine (301 +/- 193 vs. 222 +/- 87 pg/ml, p < 0.001), renin activity (3.0 +/- 3.7 vs. 1.2 +/- 1.2 ng/ml per h, p < 0.001), arginine vasopressin (1.9 +/- 6.9 vs. 0.7 +/- 0.3 pg/ml, p < 0.001) and atrial natriuretic peptide (75 +/- 75 vs. 21 +/- 9 pg/ml, p < 0.001) values ranged from normal to very high, indicating a wide spectrum of neurohumoral activation. Activation of one system did not correlate with activation of another. The clinical and laboratory variables most closely associated with neurohumoral activation were Killip class, left ventricular ejection fraction, age and use of diuretic drugs. The association between neurohumoral activation and clinical and laboratory variables varied from one neurohormone to another. CONCLUSIONS: Neurohumoral activation occurs in a significant proportion of patients at the time of hospital discharge after infarction. Which neurohormone is activated and which clinical and laboratory variables determine this activation vary from one neurohormone to another.

Aged↗

PubMed1991

[Relaxation and diastolic filling precisely evaluated in patients with left ventricular dysfunction].

To assess left ventricular (LV) diastolic function in patients with LV dysfunction, LV pressures (manometer tip) and biplane angiograms were analyzed for 27 patients with LV systolic dysfunction (EF < or = 0.45) (dilated cardiomyopathy or coronary artery disease) and 18 normal controls. LV volumes were obtained from frame-by-frame analyses of angiograms. LV relaxation was assessed by the time constant (T) of LV pressure decay. LV relaxation was impaired in patients with LV dysfunction, however, early diastolic filling assessed by the peak filling rate (PFR) and mean filling rate (MFR) during the rapid filling phase was maintained. Compared to the control group, early diastolic filling was significantly decreased in patients with LV dysfunction without mitral regurgitation (MR), but not in those with LV dysfunction with MR. In conclusion, although diastolic filling may be modified by MR, LV relaxation and early diastolic filling are essentially impaired in patients with LV dysfunction.

Adolescent↗

PubMed1987

Antiarrhythmic efficacy and hemodynamic effects of cibenzoline in patients with nonsustained ventricular tachycardia and left ventricular dysfunction.

This was a prospective single-blind, placebo-controlled study of cibenzoline in 21 patients with five or more runs of nonsustained ventricular tachycardia (VT) and left ventricular dysfunction (mean left ventricular ejection fraction 36 +/- 24%). Ambulatory electrocardiographic monitoring revealed a baseline of 616 +/- 431 runs of VT/day on placebo. Of the 18 patients tolerating the drug, 14 (77%) patients initially had a 75% or greater reduction in VT (177 +/- 164 runs of VT/day, p less than .05). A repeat ambulatory electrocardiogram documented long-term suppression of VT in 13 of 14 patients at 1 month (2.1 +/- 1.3 runs VT/day, p less than .01), in 10 of 14 patients at 3 months (2.5 +/- 1.9 runs VT/day, p less than .01), and in nine of 14 patients at 6 months (1.5 +/- 0.8 runs VT/day, p less than .01). Aggravation of arrhythmia or drug failure was seen in four of 18 (22%) patients (new onset of sudden cardiac death, two patients; sustained VT, two patients). Hemodynamic measurements were obtained with the use of right heart catheterization in patients at rest and exercising during the placebo phase and after 60 hr of oral cibenzoline. Group hemodynamic variables, both measured and derived, showed no detrimental effect of cibenzoline. However, in three of 21 patients (mean ejection fraction 21%), cibenzoline was discontinued due to severe depression of left ventricular function. Caution is recommended in the use of cibenzoline in patients with left ventricular ejection fractions of less than 25%.

Aged↗

PubMed1991

Does ventricular dysfunction occur during liver transplantation?

In conclusion, we believe that ventricular dysfunction occurs infrequently during liver transplantation, except for the very short period of "cardioplegia" of the heart on reperfusion in some patients. There is no evidence that prolonged cardiac dysfunction is a common problem during liver transplantation. Understanding the physiologic changes that occur during liver transplantation should allow the anesthesiologist to correct many factors that might otherwise cause hemodynamic instability.

Heart Diseases↗

PubMed1989

[Successful repair of tetralogy of Fallot with severe right ventricular dysfunction using veno-arterial bypass in an adult].

A 35-year-old male with tetralogy of Fallot, who had undergone left Blalock-Taussig shunt at ten year old, developed severe dysfunction of right ventricle with decreased right ventricular ejection fraction of 25% and frequent premature ventricular contractions of right ventricular origin. Following intracardiac procedure, the venoarterial assist circulation was successfully employed for 9 hours, until his hemodynamic conditions were improved. This experience reemphasized the importance of right ventricular protection and mechanical circulatory assist in the surgical treatment of Fallot's tetralogy in older children and adults who developed severe right ventricular dysfunction as a natural history of this disease.

Adult↗

PubMed2001

[ACE inhibition in patients with myocardial infarct and ventricular dysfunction: inappropriate application of therapy standards in patient samples].

Several reports indicate the benefit of ACE inhibitors for patients with left ventricular systolic dysfunction after acute myocardial infarction (MI). We sought to determine the implementation of the treatment guidelines in patient samples from the general population. Furthermore we aimed to identify patient characteristics associated with the use of ACE inhibitors. Screening of two MI-registries allowed the identification of 226 MI patients with left ventricular dysfunction. Patients were considered to be eligible for ACE inhibitor therapy when a EF < or = 40% was documented in the patient records of cardiac rehabilitation clinics (REG-MI, n = 147) or detected by standardised echocardiography (KORA, n = 78). On average 5.5 years following MI, a standardised questionnaire and a detailed medical history was obtained. Specifically, information was collected regarding current medication and potential contraindications for ACE inhibitors. MI patients with LV dysfunction received ACE inhibitors in 62% (REG-MI) and 45% (KORA). The doses prescribed were substantially smaller than target doses used in the large-scale studies (REG-MI: 40 +/- 4%, KORA: 23 +/- 3%, % of target doses). Only 13% (REG-MI) and 3% (KORA) received more than 50% of the target dosage. Additionally, actual doses of the most frequently used ACE inhibitors were significantly different (captopril: 23 +/- 2%, enalapril: 42 +/- 5% of target doses). The likelihood of receiving ACE inhibitors was significantly higher in patients with written recommendation for such medication (odds ratio 6.02, confidence interval 1.93-20.16) and in patients visiting cardiologists (odds ratio 3.69, confidence interval 1.26-11.07) as revealed by multivariate analysis of the REG-MI database. Despite national and international guidance, a large proportion of MI patients with left ventricular dysfunction is not receiving ACE inhibitors, and when used, the doses prescribed are markedly smaller than target doses used in clinical trials that established the utility of these drugs. Medical care by cardiologists and written recommendation of ACE inhibition in patient records were independent predictors of a more appropriate prescription of ACE inhibitors.

Aged↗

PubMed1998

Prognostic value of the amount of dysfunctional but viable myocardium in revascularized patients with coronary artery disease and left ventricular dysfunction. Investigators of this Multicenter Study.

OBJECTIVES: The purpose of our study was to assess the prognostic importance of the amount of dysfunctional but viable myocardium in revascularized patients with coronary artery disease (CAD) and left ventricular (LV) dysfunction. BACKGROUND: The amount of dysfunctional but viable myocardium predicts the functional improvement after revascularization and may offer more precise risk stratification of patients referred for bypass surgery or coronary angioplasty. METHODS: Two hundred and seventy-four consecutive patients with CAD and LV ejection fraction < or =40% underwent low-dose dobutamine echocardiography for viability assessment. One hundred and thirty-three of them were revascularized using either coronary artery bypass surgery (118 patients) or coronary angioplasty (15 patients) and entered this study. To quantify the amount of dysfunctional but viable myocardium, wall motion was scored using 16-segment model. The dysfunctional segments were defined as viable if they exhibited improvement in their thickening by at least 1 grade with dobutamine infusion. The patients were followed up for a mean period of 20+/-12 months (range, 2 to 48) for cardiac mortality and nonfatal cardiac events including myocardial infarction, unstable angina pectoris requiring hospitalization and hospitalization for heart failure. Standard follow-up echocardiography was performed 3 to 6 months after revascularization. RESULTS: Twenty-nine patients exhibited a large amount of dysfunctional but viable myocardium (> or =6 segments, group A), 60 patients had a small amount of dysfunctional but viable myocardium (2 to 5 segments, group B) and 44 patients were found to have dysfunctional myocardium irreversibly damaged (group C). Similar prerevascularization LV ejection fractions of 35%+/-5%, 34%+/-4%, 36%+/-4% in groups A, B and C increased to 47%+/-6% (p < 0.01 vs. baseline, p < 0.01 vs. groups B and C), to 40%+/-5% (p < 0.01 vs. baseline) and to 37%+/-6% (p = NS vs baseline), respectively, after revascularization. The greatest functional improvement after revascularization in group A patients was accompanied by a lower rate of cardiac events during follow-up (2 vs. 18 in group B, p < 0.05, and vs. 17 in group C, p < 0.01) and better cardiac event-free survival according to Kaplan-Meier survival analysis (p < 0.05 vs. groups B and C, respectively). CONCLUSION: In revascularized patients with CAD and moderate or severe LV dysfunction, the presence of a large amount of dysfunctional but viable myocardium identifies patients with the best prognosis.

Adult↗

PubMed2004

Prediction of subclinical left ventricular dysfunction with strain rate imaging in patients with asymptomatic severe mitral regurgitation.

This study sought the ability of strain rate imaging to detect subclinical left ventricular dysfunction, as evidenced by reduced contractile reserve (CR) in 32 asymptomatic patients with isolated severe mitral regurgitation. Compared with CR- patients (n = 10), CR+ patients (n = 22) had significantly higher end-systolic strain and peak systolic strain rate, but these parameters were not significantly different between CR+ patients and matched normal controls.

Aged↗

PubMed1982

The stunned myocardium: prolonged, postischemic ventricular dysfunction.

Myocardial ischemia has, for many decades, been viewed as an all-or-none process that causes myocardial necrosis when prolonged and severe, but whose effects are transient when it is brief or mild. In view of the evidence that the ischemic process may "hit, run and stun," perhaps our thinking about the consequences of myocardial ischemia should be expanded. According to this formulation, an ischemic insult not of sufficient severity of duration to produce myocardial necrosis may acutely affect myocardial repolarization and cause angina (hit); but these changes wane rapidly (run), when the balance between myocardial oxygen supply and demand has been reestablished. However, the ischemia may interfere with normal myocardial function, biochemical processes and ultrastructure for prolonged periods (stun). The severity and duration of these postischemic changes depend on the length and intensity of the ischemia, as well as on the condition of the myocardium at the onset of the ischemic episode. Furthermore, it is likely that when the myocardium is repeatedly stunned, it may exhibit chronic postischemic left ventricular dysfunction, an ill-defined condition. If prolonged, chronic postischemic left ventricular dysfunction can progress to myocardial scarring and ischemic cardiomyopathy, it may be important to determine how often it can be ameliorated by permanent improvement of myocardial perfusion by surgical treatment.

Adenosine Triphosphate↗