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Biomedical subjects

José M García-Pinilla

Publications and source records attributed to José M García-Pinilla.

8 recordsLinked to original sources
PubMed2006

[Effect of statin treatment begun early after acute myocardial infarction on endothelial function in patients with normal levels of cholesterol. VAATOPE Study (VAlue of ATOrvastatin in Postinfarction Endothelium)].

BACKGROUND AND OBJECTIVE: Recent studies have suggested that statins reduce the rate of subsequent coronary events when these drugs are indicated early alter an acute coronary event. One potential mechanism by which these drugs might reduce the likelihood of such events is by enhancing endothelial function. The aim of this study was to determine whether early cholesterol reduction with atorvastatin improved endothelial function after acute myocardial infarction in patients with normal cholesterol levels. PATIENTS AND METHOD: Patients with a first acute myocardial infarction and normal levels of cholesterol were assigned to treatment with 10 mg atorvastatin (n = 15) or placebo (n = 15) for 8 weeks. Patients who had previously received treatment with statins were excluded. Brachial ultrasound was used to measure endothelium-dependent flow-mediated dilation and response to endothelium-independent nitroglycerin. Total and LDL cholesterol levels and the distribution of risk factors were similar on admission and before randomization in both groups. All patients were assessed between 5 and 7 days postinfarction and after 8 weeks. RESULTS: Total and LDL cholesterol levels were significantly decreased after atorvastatin treatment. Total cholesterol decreased by 11% (p < 0.01) and LDL cholesterol by 18% (p < 0.01). Without atorvastatin flow-mediated dilation was unchanged (mean [SEM] 9.3 [1.7%] to 10.6 [1.7%]) but it increased with atorvastatin (8.9 [1.4%] to 16.5 [1.7%], p < 0.05). The response to nitroglycerin was similar in both groups during the period of study. CONCLUSIONS: The early administration of atorvastatin appears to enhance endothelial function in patients with acute myocardial infarction and normal levels of cholesterol.

Aged↗
PubMed2006

[Treatment of heart failure due to systolic dysfunction].

Heart failure due to systolic dysfunction is a clinical syndrome that is characterized by the appearance of the signs or symptoms of heart failure in the presence of structural heart disease that has led to decreased left ventricular contractility. Current clinical practice guidelines emphasize the importance of diagnosing and treating left ventricular dysfunction in patients without symptoms of heart disease. It is essential that currently available scientific findings are taken into account when treating all patients seen with this condition, from dietary advice to use of the most sophisticated devices. We do not know the precise treatment responses of patient belonging to subgroups that were underrepresented in large clinical trials. The present article, written after the recent publication of European and American clinical practice guidelines, provides a summary of recommended medical treatment for patients with heart failure due to systolic dysfunction.

Adrenergic beta-Antagonists↗
PubMed2006

[Effect of exercise on systolic left ventricular outflow velocity in healthy adults].

The occurrence of exercise-induced dynamic obstruction of the left ventricular outflow tract in patients without cardiomyopathy has recently been reported. However, it is not known if this phenomenon is a normal response to exercise in healthy adults. We studied 23 healthy adults using exercise Doppler echocardiography. We measured the left ventricular outflow velocity at rest and after maximum tolerated exercise. After a mean exercise duration of 12 min 45 s (2 min 32 s), the heart rate was 97.61 (6.71)% of the theoretical maximum. Left ventricular outflow velocity increased from 1.07 (0.18) m/s (range: 0.77-1.44 m/s) to 1.58 (0.35) m/s (range: 1.09-2.4 m/s). In healthy adults, exercise increased the left ventricular outflow velocity by 50%, though in no subject was it greater than 2.5 m/s. This observation appears to rule out the possibility that a high intraventricular pressure gradient is a normal response to exercise in healthy adults.

Adult↗
PubMed2004

[Update in arrhythmogenic right ventricular cardiomyopathy: genetic, clinical presentation and risk stratification].

Arrhythmogenic right ventricular cardiomyopathy (ARVC), or dysplasia, is a genetic heart muscle disease whose diagnosis is often a challenge for the clinician. It is one of the commonest causes of sudden cardiac death in the young. The classic description of the disease describes the end stage of a process where the myocardium, mainly of the right ventricle, has been substituted by fibrofatty tissue. Thus the early stages of the disease with subtle symptomatology are often missed. Unfortunately the risk of a fatal outcome is no less severe. The genetic basis is under investigations. Disease causing mutations in important cell adhesion genes (plakoglobin, desmoplakin) provide the basis for improved diagnosis and understanding of the pathogenesis. Animal models support the pathogenic theory that alterations on the integrity of the adhesion junction is followed by a cellular death and progressive fibrofatty replacement, the substrate for ventricular arrhythmias. Due the growing complexity and numerous phenotypic variations reported, sometimes in the same family, international registries have been created. The present review aims to summarise the current concepts on ARVC emphasising the genetic studies, the diagnosis, new diagnostic techniques and prognosis.

Arrhythmogenic Right Ventricular Dysplasia↗