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Biomedical subjects

Carol Chen-Scarabelli

Publications and source records attributed to Carol Chen-Scarabelli.

18 recordsLinked to original sources
PubMed2007

Peripartum cardiomyopathy: a comprehensive review.

Peripartum cardiomyopathy (PPCM) is a rare disorder in which left ventricular dysfunction and symptoms of heart failure occur in the peripartum period in previously healthy women. Incidence of PPCM ranges from 1 in 1300 to 1 in 15,000 pregnancies. The etiology of PPCM is unknown, but viral, autoimmune, and idiopathic causes may contribute. The diagnostic criteria are onset of heart failure in the last month of pregnancy or in first 5 months postpartum, absence of determinable cause for cardiac failure, and absence of a demonstrable heart disease before the last month of pregnancy. Risk factors for PPCM include advanced maternal age, multiparity, African race, twinning, gestational hypertension, and long-term tocolysis. The clinical presentation of patients with PPCM is similar to that of patients with dilated cardiomyopathy. Early diagnosis and initiation of treatment are essential to optimize pregnancy outcome. Treatment is similar to medical therapy for other forms of dilated cardiomyopathy. About half the patients of PPCM recover without complications. The prognosis is poor in patients with persistent cardiomyopathy. Persistence of disease after 6 months indicates irreversible cardiomyopathy and portends worse survival.

Adult↗
PubMed2006

Effect of clopidogrel plus aspirin on ST segments in patients with ST-elevation acute myocardial infarction.

Spontaneous ST-segment resolution (STR) after acute ST-elevation myocardial infarction is associated with favorable outcomes. Effect on STR of newer, more powerful antiplatelet and antithrombotic agents is unclear. The aim of this study was to identify independent clinical and angiographic predictors of STR in patients with ST-elevation acute myocardial infarction before percutaneous coronary intervention. We studied 206 patients admitted with ST-elevation acute myocardial infarction, of whom 37 (18%) had STR. There were 12 deaths (5.8%) that occurred in the group without spontaneous STR. Patients with spontaneous STR were younger (55 vs 61 years old, p = 0.02), had shorter duration of symptoms (117 vs 212 minutes, p <0.0001), had preserved ejection fraction (55% vs 40%, p <0.0001), had shorter hospital stays, and had lower in-hospital arrhythmias or death. Independent predictors of STR, identified by stepwise logistic regression analysis, were early clopidogrel administration (odds ratio [OR] 2.10, 95% confidence interval [CI] 1.00 to 4.40, p = 0.045), single-vessel disease (OR 2.85, 95% CI 1.22 to 6.70, p = 0.02), chest pain duration (OR 0.98, 95% CI 0.98 to 0.99, p <0.0001), collaterals (OR 4.3, 95% CI 1.7 to 10.8, p = 0.002), circumflex as a culprit vessel (OR 4.74, 95% CI 1.5 to 14.95, p = 0.008), and coronary thrombus noted on angiography (OR 5.76, 95% CI 1.63 to 20.4, p = 0.006). In conclusion, early clopidogrel administration is associated with, and likely causal for, STR. Patients with thrombus, collateral flow, and circumflex culprit vessel are more likely to have STR. In addition, our study confirms previous findings that patients with STR have preserved left ventricular function and better hospital outcomes compared with those without STR.

Aspirin↗
PubMed2006

Clinical implications of apoptosis in ischemic myocardium.

Apoptosis, a genetically programmed form of cell death, contributes to myocyte cell loss in a variety of cardiac pathologies, including cardiac failure and those related to ischemia/reperfusion injury. The apoptotic program is complex, involving both pro- and anti-apoptotic proteins, and apoptosis occurs when the equilibrium between these opposing factors is perturbed. Some of these factors are intrinsic to the apoptotic pathway, such as the pro- and anti-apoptotic members of the Bcl2 family. Other, extrinsic, cellular factors can also modify the outcome of the response to an apoptotic stimulus. In this review, we have focused on some of these extrinsic factors, such as STAT-1 as a pro-apoptotic agent and the urocortins and Bag-1 as anti-apoptotic factors, since these may be potential therapeutic targets. In addition, we discuss the profound cytoprotective effects of the antibiotic, minocycline.

Animals↗
PubMed2006

Suboptimal glycemic control, independently of QT interval duration, is associated with increased risk of ventricular arrhythmias in a high-risk population.

BACKGROUND: Although cardiovascular disease is the leading cause of mortality in diabetic patients, little is known about the impact of glycemic control on ventricular tachycardia (VT). OBJECTIVE: To investigate whether hemoglobin A1c (HbA1c) is associated with increased incidence of VT. METHODS: A retrospective study of 336 implantable cardioverter-defibrillator patients (both diabetes mellitus (DM) and non-DM) was conducted. RESULTS: HbA1c levels between 8% and 10% had a significant association with spontaneous VT, but not with QT/QTc. CONCLUSIONS: Glycemic index is a significant predictor of spontaneous VT, independently of QT interval. Optimal glycemic control may help reduce occurrence of VT and sudden cardiac death in high-risk DM patients.

Aged↗
PubMed2005

A case of fatal ephedra intake associated with lipofuscin accumulation, caspase activation and cleavage of myofibrillary proteins.

Ephedra, a herb reported to suppress appetite and stimulate the sympathetic nervous system as well as cardiac performance, has recently been related to several adverse events, including seizure, stroke, hypertension, myocardial infarction, and sudden death. Here, we describe the case of a 45-year-old woman who died of cardiovascular collapse while taking ephedra. Tissue analysis revealed non-specific degenerative alterations in the myocardium (lipofuscin accumulation, basophilic degeneration and vacuolation of myocytes, as well as myofibrillary loss), associated with myocyte apoptosis, caspase activation, and extensive cleavage of miofibrillary proteins alpha-actin, alpha-actinin, and cardiac troponin T. Healthcare professionals are therefore urged to warn their patients about the risk of serious adverse effects, which may follow ephedra intake.

Apoptosis↗
PubMed2005

Supraventricular arrhythmias: an electrophysiology primer.

Supraventricular arrhythmias are the most wide-spread group of arrhythmias and affect all age groups. Atrial fibrillation is the most common arrhythmic disorder and is even more prevalent among the elderly. Due to their prevalence, it is imperative for the clinician to be informed about these arrhythmias and treatment considerations. This paper presents a basic review of the incidence, pathophysiology, diagnosis, and treatment of supraventricular arrhythmias, along with gender differences, and discusses important implications for the health care provider. A summary of common electrocardiogram findings in supraventricular arrhythmias is presented along with a brief overview of pharmacologic agents.

Anti-Arrhythmia Agents↗
PubMed2004

Nutritional supplementation with mixed essential amino acids enhances myocyte survival, preserving mitochondrial functional capacity during ischemia-reperfusion injury.

In patients undergoing coronary surgery, the uptake of amino acids, which has been shown to correlate with oxygen consumption, is a mechanism of cardiac adaptation to the iatrogenic ischemia-reperfusion injury associated with cardioplegic arrest. Based on these premises, we sought to determine whether oral supplementation with mixed amino acids may protect the rat heart exposed to ischemia-reperfusion and to address whether this hypothesized cardioprotection is achieved, at least in part, through preservation of the energy-producing properties of mitochondria. Sprague-Dawley rats were fed (by enteral route) a liquid diet, with or without mixed essential amino acids (daily dose of 1 g/kg) for 30 days. Hearts from anesthetized rats were perfused by the Langendorff method and randomized to 3 groups. The control group was perfused with buffer for 60 minutes; the ischemia-reperfusion control and the amino acid-treated groups were exposed to 35 minutes of ischemia, followed by 60 or 120 minutes of reperfusion. Amino acid supplements minimized infarct size (22 +/- 1.8% vs 33 +/- 2.5%; p <0.05) and occurrence of cardiomyocyte apoptosis, as assessed by co-localization of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase-3-positive staining (p <0.01). Long-term treatment with amino acids also reduced the proportion of cardiomyocytes exhibiting immunostaining for cleaved caspase-9 (p <0.01) but was ineffective on processing of caspase-8. Similar results were obtained in the whole heart by caspase activity assays (p <0.01). The lessened activation of caspase-9 detected in amino acid-treated hearts paralleled a strong reduction in mitochondrial release of cytochrome c. Adenosine triphosphate (ATP) content and rate of ATP production in isolated mitochondria were reduced by >75% in control hearts after 2 hours of reperfusion (p <0.05 vs control hearts); these values returned toward those of the control group in hearts supplemented with amino acids (p <0.01). Finally, the oxygen consumption rate in myocardial skinned bundles was markedly reduced in ischemia-reperfusion control hearts and almost normalized in amino acid-treated hearts (approximately 20% and 93% of the value for normoxic hearts; p <0.01). These results suggest that oral amino acid supplementation attenuates the extent of ischemia-reperfusion injury in the rat heart, through preservation of the mitochondria-generated production of high-energy phosphates.

Amino Acids, Essential↗
PubMed2004

Minocycline inhibits caspase activation and reactivation, increases the ratio of XIAP to smac/DIABLO, and reduces the mitochondrial leakage of cytochrome C and smac/DIABLO.

OBJECTIVES: This study is aimed at investigating the novel use of minocycline for cardiac protection during ischemia/reperfusion (I/R) injury, as well as its mechanism of action. BACKGROUND: Minocycline is a tetracycline with anti-inflammatory properties, which is used clinically for the treatment of diseases such as urethritis and rheumatoid arthritis. Experimentally, minocycline has also been shown to be neuroprotective in animal models of cerebral ischemia and to delay progression and improve survival in mouse models of neurodegenerative diseases. METHODS: We studied 62 rat intact hearts exposed to I/R and cell cultures of neonatal and adult rat ventricular myocytes. RESULTS: Minocycline significantly reduced necrotic and apoptotic cell death, both in neonatal and adult myocytes, not only when given prior to hypoxia (p < 0.001), but also at reoxygenation (p < 0.05). Moreover, in the intact heart exposed to I/R, in vivo treatment with minocycline promoted hemodynamic recovery (p < 0.001) and cell survival, with reduction of infarct size (p < 0.001), cardiac release of creatine phosphokinase (p < 0.001), and apoptotic cell death (p < 0.001). In regard to its antiapoptotic mechanism of action, minocycline significantly reduced the expression level of initiator caspases, increased the ratio of XIAP to Smac/DIABLO at both the messenger RNA and protein level, and prevented mitochondrial release of cytochrome c and Smac/DIABLO (all, p < 0.05). These synergistic actions dramatically prevent the post-ischemic induction of caspase activity associated with cardiac I/R injury. CONCLUSIONS: Because of its safety record and multiple novel mechanisms of action, minocycline may be a valuable cardioprotective agent to ameliorate cardiac dysfunction and cell loss associated with I/R injury.

Animals↗
PubMed2004

Warm blood cardioplegic arrest induces mitochondrial-mediated cardiomyocyte apoptosis associated with increased urocortin expression in viable cells.

OBJECTIVES: This study assesses the mechanisms of apoptosis in patients after on-pump coronary artery bypass graft surgery and the potential involvement of the endogenous cardiac peptide urocortin as a cardiomyocyte salvage mechanism. We have previously described the mechanisms of apoptosis after ischemia-reperfusion injury in the rat heart and shown that endogenous urocortin is cardioprotective. Here we extend these findings to the human heart exposed to ischemic-reperfusion injury. METHODS: Two sequential biopsy specimens were obtained from the right atriums of 24 patients undergoing coronary artery bypass grafting at the start of grafting and 10 minutes after release of the aortic clamp. Apoptosis was identified by means of immunocytochemical colocalization between terminal deoxynucleotidyl transferase-mediated nick end-labeling positivity and active caspase-3. Immunostaining for active caspase-9 and caspase-8 was performed to identify the pathways of apoptosis induction. Urocortin and adenosine triphosphate-dependent potassium channel expression was also assessed by means of immunocytochemistry. RESULTS: Myocyte apoptosis (<0.1% before coronary artery bypass grafting) was increased after coronary artery bypass grafting and reperfusion and was greater in patients with longer periods of cardioplegic arrest (3.3% +/- 0.5% with <55 minutes and 5.1% +/- 0.9% with 85-100 minutes, P <.001). Processing of caspase-9 was always more pronounced than that of caspase-8 (P <.05). Cardioplegic arrest was also associated with increased urocortin expression (up to 29% +/- 3.5% vs <3% in samples obtained before coronary artery bypass grafting, P <.001) but only in nonapoptotic myocytes. These and surrounding viable myocytes also showed increased Kir6.1 adenosine triphosphate-dependent potassium channel expression. CONCLUSIONS: Cardioplegic arrest and subsequent reperfusion result in cardiomyocyte apoptosis, largely through mitochondrial injury, as well as exclusive urocortin expression in viable cells. This finding might suggest a cardioprotective role for endogenous urocortin in human subjects.

Apoptosis↗