Determinants of left ventricular systolic function recovery after an acute coronary syndrome.

INTRODUCTION: Ischemic heart disease is a major cause of heart failure in western societies. However, the factors that may influence left ventricular function (LVF) recovery after an acute coronary syndrome (ACS) are still unclear. OBJECTIVE: To identify variables that may influence LVF evolution one year after ACS. METHODS: 104 patients hospitalized with ACS between 7/1/2001 and 12/31/2002 and with systolic dysfunction--defined as an echocardiographic ejection fraction (EF) < or = 45%--were randomly allocated to a planned coronary follow-up program (FUP) or a general cardiology clinic (GC); patients from both groups were also randomly referred to a structured cardiac rehabilitation program (CRP). EF was re-assessed at one year. We compared differences between patients who recovered left ventricular function (EF > 45%; group 1) and those who did not (group 2). RESULTS: One year after discharge, 44.2% of the patients had recovered function. There were no significant differences between the groups in gender (77.7 vs. 76.5% male), age (56 vs. 59 years), hypertension, diabetes, dyslipidemia, smoking habits or family history. A previous history of cardiovascular events was more frequent in group 2 (11.1% vs. 35.3%, p = 0.03). Cardiac catheterization was performed before discharge in 88.8% and 88.2% in groups 1 and 2 respectively (p = NS); no differences were found in coronary anatomy between the two groups. Angioplasty was performed in 54.2% in group 1 and 50% in group 2 (p = NS). There were no differences in the use of angiotensin-converting enzyme inhibitors (83.3% vs. 87.5%), beta-blockers (87.5% vs. 87.5%), nitrates (37.5% vs. 33.3%), aspirin (95.8% vs. 95.8%), statins (79.1% vs. 75%) or diuretics (20.8% vs. 45.8%). There was no significant difference in LVF recovery between patients randomized to FUP or GC (38.5% vs. 54.5%). 87.5% of patients who completed the CRP had normal EF at one year compared to 32.7% of patients not referred to the program (p = 0.009). Although EF improved in both groups, this improvement was greater in patients who completed a CRP (EF 8% vs. 5%, p = 0.003). CONCLUSION: A previous cardiovascular event and completion of a CRP were the only variables that influenced LVF recovery. Thus, enrollment in a CRP, in addition to standard therapy, could be an important therapeutic measure in patients with systolic dysfunction after ACS; our data suggest that these programs should be more widely used.     

Effects of intravenous L-acetylcarnitine on retinal oscillatory potentials

L-acetylcarnitine is a compound with cholinergic properties and putative action on the visual system and the glucose metabolism. Ten healthy, emmertropic volunteers (age range: 21 to 28 years) were studied. Each subject was administered 5, 10, and 30 mg/kg acute intravenous doses of L-acetylcarnitine and matching placebo. Retinal oscillatory potentials to full-field flash stimulation were recorded before and 30, 60, and 120 min after administration. A systematic reduction of the implicit time of the P2 and N2 oscillatory potential components was observed after administration of the 10 and 30 mg/kg doses: significant changes were not evident at the 5 mg dose or after placebo. The latency reduction was significantly correlated with the postdrug increment of the L-acetylcarnitine plasma concentration. No other systematic modification in latency of amplitude was observed.The results were presented in part at the XXV I.S.C.E.V. Symposium, Sarasota (Florida), April 26–30, 1987.     

Correlation with age and sex of flash-evoked electroretinogram and retinal oscillatory potentials recorded with skin electrodes

Electroretinograms and retinal oscillatory potentials to full-field flash stimulation were recorded by dermal electrodes in a population of subjects (1 to 84 yrs) balanced for age and sex (119 females, 133 males), without evidence or history of ocular and/or relevant systemic diseases. The electroretinogram latencies and b-wave amplitude increased, while the a-wave amplitude decreased linearly with age. The oscillatory potential amplitude initially increased, to decrease approximately at the age of 50, with an inverted U-shaped distribution.Presented in part at the XXV ISCEV Symposium, Sarasota (Florida), April 26–30, 1987.     

The spectrum of cardiovascular abnormalities in autosomal dominant polycystic kidney disease: a 10-year follow-up in a five-generation kindred.

Clinical, electrocardiographic and echocardiographic data were collected in a group of 228 patients with autosomal dominant polycystic kidney disease (PKD) and in another group of 146 unaffected members (NPKD) both comprised in a five-generation kindred followed for 10 years, in order to determine the profile and prevalence of cardiovascular derangement of the genetic disease. A family of 181 members was used as a control. The prevalence of left ventricular hypertrophy in the three groups was 24, 14 and 6% respectively (p less than 0.01); after 10 years it increased up to 35, 26 and 13% respectively (p less than 0.05). The evidence of mitral-valve prolapse was more frequent in PKD and in NPKD group (25 and 20% respectively) than in control subjects (2%) (p less than 0.0001). Mitral incompetence was found in 30, 18 and 8% of those groups respectively (p less than 0.002). The large difference in mitral involvement did not change over time. Tricuspid valve prolapse was detected in 5, 4 and 1% of the three groups, respectively (p less than 0.05). A small increase in frequency was found after 10 years only in polycystic kidney disease patients. Regurgitant aortic lesions were present in higher prevalence in PKD (19%) and NPKD (17%) members than in controls (5%) (p less than 0.001). After 10 years they were 23, 20 and 8%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Carvedilol protects ischemic cardiac mitochondria by preventing oxidative stress.

Ischemia negatively affects mitochondrial function by inducing the mitochondrial permeability transition (MPT). The MPT is triggered by oxidative stress, which occurs in mitochondria during ischemia as a result of diminished antioxidant defenses and increased reactive oxygen species production. It causes mitochondrial dysfunction and can ultimately lead to cell death. Therefore, drugs able to minimize mitochondrial damage induced by ischemia may prove to be clinically effective. We analyzed the effect of carvedilol, a beta-blocker with antioxidant properties, on mitochondrial dysfunction. Carvedilol decreased levels of TBARS (thiobarbituric acid reactive substances), an indicator of oxidative stress, which is consistent with its antioxidant properties. Regarding cell death by apoptosis, although ischemia did increase caspase-8-like activity, there were no changes in caspase-3-like activity, which is activated downstream of caspase-8; this may indicate that the apoptotic cascade is not activated by 60 minutes of ischemia. We conclude that carvedilol protects ischemic mitochondria by preventing oxidative mitochondrial damage, and, by so doing, it may also inhibit the formation of the MPT pore.