Coronary Artery Disease: Elliott P

Kaski JP, Elliott P, Anonymous00045. · The Heart Hospital, University College London, UK. · Herz. · Pubmed #17882369 No free full text.

Abstract: In the WHO/ISFC classification of 1996, cardiomyopathies were defined as primary myocardial disorders of unknown cause. Heart muscle disorders of known etiology or associated with systemic disorders were classified as secondary or specific heart muscle diseases. An expert panel of the American Heart Association has recently suggested a new scheme that combines genetic and clinical criteria. In this system, the term primary is used to describe cardiac diseases in which the heart is the sole or predominantly involved organ and secondary to describe diseases in which myocardial dysfunction is part of a systemic disorder. In a radical departure from convention, they also suggested that ion channelopathies and disorders of conduction should be considered cardiomyopathies as well. The ESC Working Group on Myocardial and Pericardial Diseases has taken a different approach based on the belief that a clinically oriented classification system in which heart muscle disorders are grouped according to ventricular morphology and function remains the clinically most useful method for diagnosing and managing patients and families with heart muscle disease. In the ESC position statement, cardiomyopathies are defined as myocardial disorders in which the heart muscle is structurally and functionally abnormal, in the absence of coronary artery disease, hypertension, valvular disease and congenital heart disease sufficient to cause the observed myocardial abnormality. In this article, this is illustrated by examples of dilated cardiomyopathy as familial/genetic forms and nonfamilial/nongenetic forms.

Elliott P, O'Hare R, Bill KM, Phillips AS, Gibson FM, Mirakhur RK. · Department of Clinical Anaesthesia, Royal Victoria Hospital. Belfast, United Kingdom. · Anesth Analg. · Pubmed #10866887 links to  free full text

Abstract: We compared the hemodynamic effects of a bolus administration of 1 microg/kg remifentanil for 1, 3, and 5 min (1, 0.33, and 0.2 microg. kg(-1). min(-1), respectively) in patients scheduled for coronary artery bypass grafting anesthetized with small-dose propofol. The study was terminated after only eight patients had been enrolled (three received remifentanil at a rate of 1.0 microg. kg(-1). min(-1), two at 0.33 microg. kg(-1). min(-1), and three at 0.2 microg. kg(-1). min(-1)) because of severe hemodynamic instability, which was particularly marked in four patients and consisted of severe bradycardia in one patient and severe hypotension with a reduction in systemic vascular resistance in three others. One patient showed evidence of myocardial ischemia. All patients responded to therapeutic interventions. The results show that remifentanil should be given only by slow infusion to such patients. IMPLICATIONS: This study investigates the effect on the heart and blood vessels of various rates of administration of boluses of a relatively new potent opiate, remifentanil, to patients with coronary artery disease. The results show that remifentanil should be given only by slow infusion to such patients.

McCourt KC, Elliott P, Mirakhur RK, McMurray TJ, Phillips AS, Cochrane D. · Department of Anaesthetics, Queen's University, Belfast, Ireland, UK. · Br J Anaesth. · Pubmed #10690133 links to  free full text

Abstract: We have assessed the haemodynamic effects of rapacuronium (Org 9487) in adults undergoing cardiac surgery and compared these with vecuronium and placebo. We studied 56 adult patients undergoing coronary artery bypass grafting or valve replacement surgery using a fentanyl-based anaesthetic technique. A pulmonary artery flotation catheter was inserted before induction of anaesthesia. After induction, tracheal intubation and stabilization of haemodynamic measurements, subjects were allocated randomly to receive rapacuronium 1.5 mg kg-1 vecuronium 0.1 mg kg-1 or saline placebo. Haemodynamic measurements were made before drug administration and 1, 3, 5 and 10, and if possible, 15 min after administration. Rapacuronium was associated with statistically significant increases in heart rate (17%) and cardiac index (15%) and decreases in mean arterial pressure (11%) and systemic vascular resistance (18%), whereas vecuronium and placebo were associated with significant decreases in heart rate only (14-15%) (P < 0.05). No cutaneous signs of histamine release were observed. Clinically, the results were within acceptable limits. Our results suggest that administration of rapacuronium may be associated with significant changes in heart rate and arterial pressure in patients undergoing coronary artery bypass grafting.

Elliott P, Andersson B, Arbustini E, Bilinska Z, Cecchi F, Charron P, Dubourg O, Kühl U, Maisch B, McKenna WJ, Monserrat L, Pankuweit S, Rapezzi C, Seferovic P, Tavazzi L, Keren A. · Hadassah University Hospital Ein Kerem, Kirjat Hadassah, Jerusalem 91120, Israel. · Eur Heart J. · Pubmed #17916581 links to  free full text

Abstract: In biology, classification systems are used to promote understanding and systematic discussion through the use of logical groups and hierarchies. In clinical medicine, similar principles are used to standardise the nomenclature of disease. For more than three decades, heart muscle diseases have been classified into primary or idiopathic myocardial diseases (cardiomyopathies) and secondary disorders that have similar morphological appearances, but which are caused by an identifiable pathology such as coronary artery disease or myocardial infiltration (specific heart muscle diseases). In this document, The European Society of Cardiology Working Group on Myocardial and Pericardial Diseases presents an update of the existing classification scheme. The aim is to help clinicians look beyond generic diagnostic labels in order to reach more specific diagnoses.

Limongelli G, Pacileo G, Marino B, Digilio MC, Sarkozy A, Elliott P, Versacci P, Calabro P, De Zorzi A, Di Salvo G, Syrris P, Patton M, McKenna WJ, Dallapiccola B, Calabro R. · Second University of Naples, Monaldi Hospital, Naples, Italy. · Am J Cardiol. · Pubmed #17697839 No free full text.

Abstract: The aim of this study was to characterize cardiovascular involvement in a large number of patients with LEOPARD syndrome. Twenty-six patients (age range 0 to 63 years, median age at the time of the study evaluation 17 years) underwent clinical and genetic investigations. Familial disease was ascertained in 9 patients. Nineteen patients (73%) showed electrocardiographic abnormalities. Left ventricular (LV) hypertrophy was present in 19 patients (73%), including 9 with LV outflow tract obstructions; right ventricular hypertrophy was present in 8 patients (30%). Valve (57%) and coronary artery (15%) anomalies were also observed. Single patients showed LV apical aneurysm, LV noncompaction, isolated LV dilation, and atrioventricular canal defect. During follow-up (9.1 +/- 4.5 years), 2 patients died suddenly, and 2 patients had cardiac arrest. These patients had LV hypertrophy. Despite the limited number of subjects studied, genotype-phenotype correlations were observed in familial cases. In conclusion, most patients with LEOPARD syndrome showed LV hypertrophy, often in association with other valvular or congenital defects. A spectrum of underrecognized cardiac anomalies were also observed. Long-term prognosis was benign, but the occurrence of 4 fatal events in patients with LV hypertrophy indicates that such patients require careful risk assessment and, in some cases, consideration for prophylaxis against sudden death.