Biomedical subjects

Jordi Soler-Soler

Publications and source records attributed to Jordi Soler-Soler.

58 records · Page 4Linked to original sources

PubMed2002

Hypoxia and acidosis impair cGMP synthesis in microvascular coronary endothelial cells.

To characterize the effects of ischemia on cGMP synthesis in microvascular endothelium, cultured endothelial cells from adult rat hearts were exposed to hypoxia or normoxia at pH 6.4 or 7.4. Cellular cGMP and soluble (sGC) and membrane guanylyl cyclase (mGC) activities were measured after stimulation of sGC (S-nitroso-N-acetyl-penicillamine) or mGC (urodilatin) or after no stimulation. Cell death (lactate dehydrogenase release) was negligible in all experiments. Hypoxia at pH 6.4 induced a rapid approximately 90% decrease in cellular cGMP after sGC and mGC stimulation. This effect was reproduced by acidosis. Hypoxia at pH 7.4 elicited a less pronounced (approximately 50%) and slower reduction in cGMP synthesis. Reoxygenation after 2 h of hypoxia at either pH 6.4 or 7.4 normalized the response to mGC stimulation but further deteriorated the sGC response; normalization of pH rapidly reversed the effects of acidosis. At pH 7.4, the response to GC stimulation correlated well with cellular ATP. We conclude that simulated ischemia severely depresses cGMP synthesis in microvascular coronary endothelial cells through ATP depletion and acidosis without intrinsic protein alteration.

Acidosis↗

PubMedDate not supplied

Do myocardial perfusion SPECT and radionuclide angiography studies in adult patients with hypertrophic cardiomyopathy have prognostic implications?

BACKGROUND: Some myocardial perfusion single photon emission computed tomography (SPECT) and radionuclide ventriculography studies have suggested that the presence of regional perfusion defects and diastolic abnormalities could have prognostic implications in patients with hypertrophic cardiomyopathy (HC). The aim of this prospective study was to analyze the prognostic value of these techniques in adult patients with HC. METHODS AND RESULTS: One hundred one patients with HC (44 women; mean age, 54 +/- 16 years; 55% obstructive) were prospectively studied by means of myocardial perfusion SPECT and radionuclide angiography. Of these patients, 55 (54.4%) had an abnormal myocardial perfusion SPECT study: 28 (27.7%) had fixed defects and 41 (40.6%) had reversible defects; 15 (14.8%) of these patients had both types of defect. Of the patients, 16% had left ventricular ejection fraction lower than 60%, 25.7% had an abnormal peak filling rate, and 51% had an abnormal time to peak filling rate. During 5.6 +/- 2.7 years of follow-up, 13 patients (12.8%) died (heart failure 8 and sudden death in 5) and 14 had one or more severe complications develop (syncope in 6, angina III-IV in 4, dyspnea III-IV in 10, and acute myocardial infarction in 3). The summed difference score was higher in patients with cardiac death (2.2 +/- 2.3 vs 1.1 +/- 1.3, P = .008), and fixed defects were more prevalent in patients with severe complications (57% vs 21%, P = .01). In the Kaplan-Meier survival plot analysis, severe complications were more likely in patients with fixed defects (P = .01) or ejection fraction lower than 60% ( P = .01). CONCLUSIONS: Prognostic information from myocardial perfusion SPECT and radionuclide angiography has limited clinical significance with regard to cardiac death in adult patients with HC. However, the presence of fixed defects and lower ejection fraction in these patients has an adverse prognostic meaning for severe complications.

Cardiomyopathy, Hypertrophic↗

PubMedDate not supplied

Effect of long-acting nifedipine on mortality and cardiovascular morbidity in patients with stable angina requiring treatment (ACTION trial): randomised controlled trial.

BACKGROUND: Calcium antagonists are widely prescribed for angina pectoris but their effect on clinical outcome is controversial. We aimed to investigate the effect of the calcium antagonist nifedipine on long-term outcome in patients with stable angina pectoris. METHODS: We randomly assigned 3825 patients with treated stable symptomatic coronary disease to double-blind addition of nifedipine GITS (gastrointestinal therapeutic system) 60 mg once daily and 3840 to placebo. The primary endpoint was the combination of death, acute myocardial infarction, refractory angina, new overt heart failure, debilitating stroke, and peripheral revascularisation. Mean follow-up was 4.9 years (SD 1.1). Analysis was by intention to treat. FINDINGS: 310 patients allocated nifedipine died (1.64 per 100 patient-years) compared with 291 people allocated placebo (1.53 per 100 patient-years; hazard ratio 1.07 [95% CI 0.91-1.25], p=0.41). Primary endpoint rates were 4.60 per 100 patient-years for nifedipine and 4.75 per 100 patient-years for placebo (0.97 [0.88-1.07], p=0.54). With nifedipine, rate of death and any cardiovascular event or procedure was 9.32 per 100 patient-years versus 10.50 per 100 patient-years for placebo (0.89 [0.83-0.95], p=0.0012). The difference was mainly attributable to a reduction in the need for coronary angiography and interventions in patients assigned nifedipine, despite an increase in peripheral revascularisation. Nifedipine had no effect on the rate of myocardial infarction. INTERPRETATION: Addition of nifedipine GITS to conventional treatment of angina pectoris has no effect on major cardiovascular event-free survival. Nifedipine GITS is safe and reduces the need for coronary angiography and interventions.

Angina Pectoris↗

PubMedDate not supplied

Transesophageal echocardiography in the diagnosis of acute aortic syndrome.

In recent years, technological advances in echocardiography have led to improvements in the diagnosis of acute aortic disease. With transesophageal echocardiography (TEE) and, particularly, bi- and multiplane probes, the physiopathologic understanding of these diseases has widened. Thus, new entities such as penetrating ulcer and intramural hematoma have been described and differentiated from classical aortic dissection.

Acute Disease↗