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PubMed2005

Rationale for the use of angiotensin II receptor blockers in patients with left ventricular dysfunction (part I of II).

Almost 5 million individuals in the United States are diagnosed with chronic heart failure (HF), and the prevalence is increasing. Angiotensin-converting enzyme (ACE) inhibitors and beta blockers, neurohormonal antagonists that block the renin-angiotensin system (RAS) and the sympathetic nervous system, respectively, have been shown in clinical trials to reduce morbidity and mortality in patients with HF, and these therapies are now integral components of standard HF treatment. Yet, morbidity and mortality rates in HF remain unacceptably high, and the limitations of current standard therapies are becoming increasingly apparent. About 10% of patients with HF are unable to tolerate ACE inhibitors, often because of cough. In addition, ACE inhibition may not completely block the RAS because angiotensin II, the main end product of the RAS, can be generated via non-ACE enzymatic pathways. Angiotensin II receptor blockers (ARBs) may exert more complete RAS blockade than ACE inhibitors by interfering with the binding of angiotensin II at the receptor level, regardless of the enzymatic pathway of production. They are also better tolerated than ACE inhibitors and have been shown to improve symptoms and function in clinical trials in patients with HF. These factors provide a strong rationale for the study of the clinical effects of ARBs in patients with HF.

Aged↗
PubMed1996

The multifarious spectrum of ischemic left ventricular dysfunction: relevance of new ischemic syndromes.

Ischemic heart disease, once limited to a number of well defined entities such as angina of effort, unstable angina, and myocardial infarction, must now be regarded as a much more complex and elusive entity. Silent ischemia was the first of the new ischemic syndromes to be described. Recently, three further new syndromes have been added, namely stunning, hibernation and preconditioning. All three have one common theme--they can be related to ischemia and reperfusion. In stunning, there is post-reperfusion mechanical dysfunction that recovers. In hibernation, there is prominent contractile dysfunction, apparently out of proportion to the reduction in coronary flow, and the recovery upon reperfusion is good. In preconditioning, severe ischemia followed by reperfusion protects against subsequent ischemia which may modify the severity of ischemic damage in the other ischemic syndromes. Ischemic LV dysfunction as found in post-infarct patients and in the absence of any simple relation to reperfusion, can be either diastolic or systolic or both in nature. In ischemic LV diastolic dysfunction without major systolic dysfunction, calcium antagonists may be appropriate therapy which could point to a role for abnormalities in the regulation of cytosolic calcium. It is proposed that there is potentially a mixed post-infarct syndrome, which may comprise one or more of the new ischemic syndromes (silent ischemia, stunning, hibernation, and preconditioning), as well as a varying degree of systolic and/or diastolic dysfunction. The basis of the systolic dysfunction is, at least in part, post-infarct LV remodeling. Several of these entities could overlap in the same patient. The term "mixed post-infarct ischemic syndrome" is suggested to describe this condition.

Animals↗
PubMed1995

Glucose metabolism and left ventricular dysfunction are normalized by insulin and islet transplantation in mild diabetes in the rat.

The aim of the present experimental study in the rat heart was to assess cardiac performance and metabolism in mild diabetes of 2 months' duration (postprandial blood sugar levels of 307 +/- 101 mg/dl and nearly normal fasting blood glucose of 102 +/- 40 mg/dl) using the working rat heart model at physiological workload with a perfusion time of 60 min. We also compared the effect of two forms of therapy for diabetes, islet transplantation and insulin therapy (s.c.), after 2 months. A 36% reduction in glucose utilization is metabolically characteristic for the diabetic heart, mainly caused by a 55% reduced glucose uptake (P < 0.001), but also by a nearly twofold increased lactate and pyruvate production (P < 0.001). This reduced carbohydrate metabolism is accompanied by a 37% reduction of oxygen uptake (P < 0.001) as well as a significant reduction in myocardial ATP and CP levels (P < 0.001), resulting in a significantly reduced cardiac output (P < 0.001). Moreover, the balance of energy reveals that the diabetic heart obtains 46% of its energy requirements for 1 h from endogenous glycogen, whereas the control heart obtains 91% of its energy needs (i.e. preferentially) from exogenous glucose (only 9% from endogenous glycogen). Both investigated therapeutic interventions led to a complete reversibility of the hemodynamic and metabolic alterations, indicating that the cause of diabetic cardiomyopathy in this model of mild and short-term diabetes is due to a defect in cardiac carbohydrate metabolism, which is correctable by insulin administration.

Adenosine Triphosphate↗
PubMed1994

Left ventricular dysfunction in ischemic heart disease: fundamental importance of the fibrous matrix.

The contractile function of the myocardium is coordinated by a fibrous matrix of exquisite organization and complexity. In the normal heart, and apparently in physiological hypertrophy, this matrix is submicroscopic. In pathological states changes are frequent, and usually progressive. Thickening of the many elements of the fine structure is due to an increased synthesis of Type I collagen, This change, which affects the myocardium in a global manner, can be observed by light microscopy using special techniques. Perivascular fibrosis, with an increase in vascular smooth muscle, is accompanied by development of fibrous septa, with a decrease in diastolic compliance. These structural changes are believed to be due to increased activation of the renin-angiotensin-aldosterone system, and to be independent of the processes of myocyte hypertrophy. Reparative or replacement fibrosis is a separate process by means of which small and large areas of necrosis heal, with the development of coarse collagen structures, which lack a specific organizational pattern. Regarding ischemic heart disease, an increase in tissue collagenase is found in experimental myocardial "stunning" and in the very early phase of acute infarction. Absence of elements of the fibrous matrix allow for myocyte slippage, and--if the affected area is large--cardiac dilatation. If, subsequently, the necrosis becomes transmural, there is further disturbance of collagen due to both mechanical strain and continued autolysis, During healing collagen synthesis increases greatly to allow for reparative scarring in the available tissue matrix. In cases of infarction with moderate or severe initial dilatation, pathological hypertrophy of the spared myocardium is progressive, accounting for late heart failure and poor survival.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Diabetes and the occurrence of ventricular arrhythmic events in patients with severe left ventricular dysfunction.

AIMS/HYPOTHESIS: Diabetes is associated with a higher risk of ischaemic heart disease and heart failure, which frequently lead to rhythm disorders. However, experimental and clinical studies are inconsistent with regard to the risk of arrhythmic events in patients with diabetes. We studied the frequency of ventricular arrhythmic events in patients with and without diabetes. METHODS: The study group included 207 patients with severe heart failure. The severity of ventricular arrhythmias was assessed by 24-h Holter monitoring, using prospectively defined measures of ventricular arrhythmic burden. RESULTS: Patients with diabetes comprised 48% of the study group. All measures of ventricular ectopy were much lower in patients with diabetes. Mean hourly ventricular pairs (13.3+/-3.7 vs 7.2+/-2.0, p=0.03), mean hourly repetitive ventricular beats (32+/-9 vs 17+/-5, p=0.01), and the frequency of ventricular tachycardia episodes per 24 h (36+/-13 vs 16+/-6, p=0.01) were lower in patients with diabetes. After inclusion of clinical variables and drug therapies in a multivariate analysis, the negative relationship between diabetes and the frequency of ventricular pairs (p=0.03), repetitive ventricular beats (p=0.04), and ventricular tachycardia (p=0.03) remained independent. In multivariate logistic regression, the risk of developing ventricular tachycardia was lower in patients with diabetes with an adjusted odds ratio of 0.41 (95% CI, 0.22 to 0.75, p=0.004). CONCLUSION/INTERPRETATION: Diabetes confers a protective effect with regard to the occurrence of ventricular arrhythmias in the setting of decompensated heart failure. The precise mechanism of this phenomenon requires further investigation.

Arrhythmias, Cardiac↗
PubMedDate not supplied

Transient left ventricular dysfunction in childhood sickle cell disease.

For unclear reasons, myocardial infarction is rare in childhood sickle cell disease, whereas lung, bone, and brain infarcts are more common. During vasoocclusive crisis and infection, acute myocardial ischemia and chronic volume overload from anemia may result in myocardial dysfunction. We report a child who had reversible cardiac dysfunction that mimicked myocardial infarction.

Child↗
PubMed2004

Current concepts for the neurohormonal management of left ventricular dysfunction after myocardial infarction.

The importance of addressing neurohormonal activation in patients after a myocardial infarction is now well-appreciated. Inhibition of the renin-angiotensin-aldosterone axis and the sympathetic nervous system can result in improved cardiac function and survival. As we learn more about other systems, we should be able to realize further benefits. In particular, the roles of endothelin, matrix metalloproteinases, and cytokines in remodeling are being investigated, with the potential to result in better outcomes for patients.

Adrenergic beta-Antagonists↗
PubMed1995

Molecular changes of titin in left ventricular dysfunction as a result of chronic hibernation.

Cardiomyocytes of chronic hibernating myocardium are affected by partial to complete loss of sarcomeres, accumulation of glycogen, adaptations in size and shape of mitochondria, reorganisation of nuclear chromatin and depletion of sarcoplasmic reticulum. The nature of these changes, which from a purely morphologic viewpoint are akin to dedifferentiation, needed further clarification at the molecular level. For this purpose we have studied the expression and reorganization of titin, one of the earliest markers of cardiomyocytes differentiation. By use of monoclonal antibodies, recognizing different epitopes distributed over the whole length of the titin molecule, we were able to detect changes in its molecular organization as a result of chronic hibernation. The epitopes of the titin molecule attached to the Z-disc and those present close to the M-line remained detectable at all stages of hibernation, while epitopes at the A-I junction and parts of the myosin anchoring region of the molecule became masked or were lost. A fragmented or punctuated appearance of the titin staining pattern with antibodies to A-I junction related epitopes is found in cells which we consider to represent a more advanced stage of dedifferentiation. Changes in the distribution of the titin molecule or its molecular environment in hibernating myocardium resemble at least in part changes occurring during muscle cell differentiation, although in reversed order.

Animals↗
PubMed1994

Prognostic value of neurohumoral activation in patients with an acute myocardial infarction: effect of captopril.

OBJECTIVES: This study attempted to evaluate whether neurohumoral activation at the time of hospital discharge in postinfarction patients helps to predict long-term prognosis and whether long-term therapy with the angiotensin-converting enzyme inhibitor captopril modifies this relation. BACKGROUND: Neurohumoral activation persists at the time of hospital discharge in a large number of postinfarction patients. The Survival and Ventricular Enlargement (SAVE) study demonstrated that the angiotensin-converting enzyme inhibitor captopril improves survival and decreases the development of severe heart failure in patients with left ventricular dysfunction (left ventricular ejection fraction < or = 40%) but no overt postinfarction heart failure. METHODS: In 534 patients in the SAVE study, plasma neurohormone levels were measured a mean of 12 days after infarction. Patients were then randomized to receive captopril or placebo and were followed up for a mean (+/- SD) of 38 +/- 6 months (range 24 to 55). The association between activation of plasma neurohormones at baseline and subsequent cardiovascular mortality or the development of heart failure was assessed with and without adjustment for other important prognostic factors. RESULTS: By univariate analysis, activation of plasma renin activity and aldosterone, norepinephrine, atrial natriuretic peptide and arginine vasopressin levels were related to subsequent cardiovascular events, whereas epinephrine and dopamine levels were not. By multivariate analysis, only plasma renin activity (relative risk 1.6, 95% confidence interval [CI] 1.0 to 2.5) and atrial natriuretic peptide (relative risk 2.2, 95% CI 1.3 to 3.8) were independently predictive of cardiovascular mortality, whereas the other neurohormones were not. Only plasma renin activity and aldosterone, atrial natriuretic peptide and arginine vasopressin were independent predictors of the combined end points of cardiovascular mortality, development of severe heart failure or recurrent myocardial infarction. Except for 1-year cardiovascular mortality, the use of captopril did not significantly modify these relations. CONCLUSIONS: Neurohumoral activation at the time of hospital discharge in postinfarction patients is an independent sign of poor prognosis. This is particularly true for plasma renin activity and atrial natriuretic peptide. Except for 1-year cardiovascular mortality, captopril does not significantly modify these relations.

Aged↗
PubMed2005

Determinants of coronary events in patients with stable angina: results from the impact of nicorandil in angina study.

BACKGROUND: IONA was a randomized trial of nicorandil (20 mg twice daily) versus placebo in 5126 patients with stable angina of effort. We present the characteristics as measured at baseline that were found to be associated with increased risk of major outcomes. METHODS: The primary end point of the study was coronary heart disease death, nonfatal myocardial infarction (MI), or unplanned hospitalization for cardiac chest pain. The secondary outcome excluded the softer outcome of unplanned hospitalization for chest pain. Potential prognostic factors included nicorandil treatment, sex, smoking, severity of angina (Canadian Cardiovascular Society [CCS] grading), previous MI, coronary artery bypass graft/percutaneous transluminal coronary angioplasty (CABG/PTCA), left ventricular dysfunction, left ventricular hypertrophy (LVH) on electrocardiography (ECG), histories of diabetes or hypertension, baseline cardiovascular drugs, age, blood pressures, heart rate, height, weight, and body mass index. RESULTS: A total of 5047 patients had complete baseline information. There were 724 primary outcomes and 240 secondary outcomes. The strongest determinants of the hard secondary end point were CCS score (hazards ratio [HR] 2.25, 95% confidence intervals [CI] 1.50-3.38) for grades III and IV versus grade I, age (HR 1.23, 95% CI 1.13-1.33) for 5-year risk, and previous MI (HR 2.05, 95% CI 1.48-2.85). The results for the primary outcome were similar, with stronger associations with LVH on ECG and smoking, and a weaker association with age. CONCLUSIONS: We present models of risk factors for coronary outcomes in a population with angina of effort. The strongest risk factors were the CCS score and previous MI.

Aged↗
PubMed2006

MgSO4 prevents left ventricular dysfunction in an animal model of preeclampsia.

OBJECTIVE: We hypothesized that cardiac function would be reduced in a pregnant rat model of preeclampsia induced by L-NAME, a NOS inhibitor, and be reversed with magnesium sulfate prophylaxis. STUDY DESIGN: Female Sprague-Dawley rats were bred in-house. On gestational day 17, rats were anesthetized and osmotic minipumps were implanted to continuously deliver saline, L-NAME, or L-NAME and MgSO4. On gestational day 21, hearts were isolated and perfused in the working mode using Krebs Henseleit buffer. RESULTS: Pregnant rats treated with L-NAME displayed significant hypertension compared to the saline-treated controls (P < 0.05). Moreover, cardiac output and cardiac work were significantly reduced in the L-NAME-treated rats compared to controls (P < 0.05). In the L-NAME-treated rats given MgSO4, cardiac function remained normal. CONCLUSION: Cardiac function is depressed in an animal model of preeclampsia induced by L-NAME infusion. MgSO4 prevented the reduction in cardiac function and is clearly beneficial in preserving normal heart function in preeclampsia.

Animals↗
PubMed2004

Effect of perindopril on platelet nitric oxide resistance in patients with chronic heart failure secondary to ischemic left ventricular dysfunction.

In 15 patients with chronic heart failure of ischemic origin who were not previously treated with angiotensin-converting enzyme inhibitors, platelets exhibited hyperaggregability and impaired responsiveness to the antiaggregatory and cyclic guanosine monophosphate-stimulatory effects of nitric oxide donor sodium nitroprusside compared with normal subjects; this was paralleled by increased blood levels of superoxide radicals. Treatment with perindopril for 4 days significantly improved platelet responses to sodium nitroprusside; there was also a trend toward a decrease in superoxide radical levels.

Angiotensin-Converting Enzyme Inhibitors↗