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Biomedical subjects

G Sanz

Publications and source records attributed to G Sanz.

At least 127 records · Page 7Linked to original sources
PubMed1986

Clinical course and risk stratification of myocardial infarct survivors with three-vessel disease.

Prevalence of three-vessel disease was prospectively analyzed in a series of 462 consecutive infarct survivors aged 60 years or less. Eighty-seven percent (403) of the patients were catheterized within one month of the acute event, and were followed for a mean of 43 months (range 21 to 69). Three-vessel disease was present in 96 cases (24%) and these patients form the study population. The primary goals of this study were to determine the prevalence of three-vessel disease and to identify predictors of survival and new coronary events among this subset of infarct survivors. During follow-up, 15 patients died, 17 had a recurrent nonfatal infarction, and 54 developed angina (4-year probability of each cardiac event being 0.20, 0.22, and 0.59, respectively). Cox's stepwise multivariate analysis identified the ejection fraction (EF) as the only predictor of survival (p less than 0.001). No predictors for nonfatal ischemic events were found among the independent variables considered. Patients were stratified in risk categories according to the EF. Four-year probability of survival was 1.0 in participants with EF = greater than 50% (n = 23), 0.77 for those with EF = 21% to 49% (n = 66), and 0.22 in patients with more severe left ventricular dysfunction, EF = less than 20% (n = 7). Probability of occurrence of nonfatal reinfarction or angina was similar in the three risk categories. Thus, our results indicate that a normal ejection fraction is found in 25% of infarct survivors with three-vessel disease, and that this subset of patients has a low incidence of early and intermediate range coronary events.

Angina Pectoris↗
PubMed1986

Systolic compression of coronary artery in hypertrophic cardiomyopathy.

To determine the prevalence and significance of the systolic compression of the anterior descending coronary artery in hypertrophic cardiomyopathy, we studied 54 consecutive patients out of a catheterization laboratory population of 1619. This angiographic finding was found to be more prevalent (P less than 0.001) and severe in myopathic than in secondary hypertrophy. Complete systolic occlusion occurred in 5 of the 6 patients with nonobstructive cardiomyopathy showing the systolic narrowing. Severe septal squeezing was also present in these cases and the diastolic time lag to refill the distal branches reached 20-33% of the diastolic period. This subset of patients showed the least dynamic anterior wall contraction (P less than 0.001) and the highest incidence of thallium-201 perfusion defects (P less than 0.05) and of recurrent cardiac arrest (P less than 0.05). We conclude that severe systolic compression of the descending coronary artery in hypertrophic cardiomyopathy may be an angiographic marker of the myopathic hypertrophy extending to the anterior wall and might contribute to ischemia when the time to restore the distal perfusion is greatly delayed.

Adolescent↗
PubMed1984

Severe inherited "homozygous" protein C deficiency in a newborn infant.

A relapsing clinical syndrome of skin lesions and disseminated intravascular coagulation (DIC) that showed remission with the infusion of fresh frozen plasma is described in a newborn infant with homozygous deficiency of protein C antigen. This patient presented since birth a recurrent clinical picture of DIC and ecchymotic skin lesions that resembled typical ecchymosis except for the fact that they showed immediate improvement with the administration of fresh frozen plasma. Using an enzyme linked immunosorbent assay method, the determination of protein C antigen levels in the patient, without ingestion of coumarin drugs, showed very low values (less than 1%). No other deficiencies in the vitamin-K-dependent factors or in antithrombin III, antiplasmin, and plasminogen were found. Seven relatives of the infant had heterozygous deficiency in protein C antigen (values between 40-55%), without clinical history of venous thrombosis. The pedigree analysis of this family suggests an autosomal recessive pattern of inheritance for the clinical phenotype, although an autosomal dominant pattern has been postulated until now in other reported families. We conclude that our patient has a homozygous deficiency in protein C and this homozygous state may be compatible with survival beyond the neonatal period.

Blood Coagulation Disorders↗
PubMed1984

Natural history of severe left ventricular dysfunction after myocardial infarction.

The prevalence and prognosis of severe left ventricular dysfunction after infarction was prospectively analyzed in a series of 259 male patients aged 60 years or less surviving an acute myocardial infarction. All patients underwent coronary angiography 30 days after the acute event and were followed up for a mean period of 34 months (range, 15 to 55 months). Forty-five patients (17 percent) were found to have severe left ventricular dysfunction (ejection fraction less than or equal to 30 percent). Comparison of patients with and without severe impairment of left ventricular function showed the former to have a lower cardiac index (p less than 0.001), higher left ventricular end-diastolic volume index (p less than 0.001), and a higher prevalence of three-vessel disease (p less than 0.025) and of total or subtotal occlusion of at least one coronary artery (p less than 0.025). While the occurrence of congestive heart failure was higher in patients with severe left ventricular dysfunction (p less than 0.001), the probability of developing angina was similar in both groups. Cox's regression analysis showed ejection fraction to be the only independent predictor of survival in patients with severe impairment of left ventricular function. An ejection fraction of 20 percent or less identified a subset of patients with the highest mortality (62 percent at four years), significantly different from that of patients whose ejection fraction was between 21 and 30 percent (28 percent) (p less than 0.001).

Adult↗
PubMed1983

Prevalence and prognosis after a first nontransmural myocardial infarction.

Prevalence, prognosis, and coronary anatomy associated with nontransmural myocardial infarction (MI) were prospectively assessed in 458 consecutive men admitted to our coronary care unit with a first MI. Cardiac catheterization was performed in 402 of the 436 survivors within 1 month of the acute event. Mean follow-up was 33 months (range 5 to 72). Nontransmural MI was diagnosed in 28 patients (6%). These patients were younger (46 +/- 10 versus 51 +/- 7 years, p less than 0.001) and had lower peak creatine kinase values (601 +/- 319 versus 1,141 +/- 923 U, p less than 0.01) and better ejection fraction (63 +/- 8 versus 46 +/- 14, p less than 0.001) than did their counterparts. Survivors of nontransmural MI also had fewer affected arteries (p less than 0.001) and a lower prevalence of total or subtotal occlusion (greater than 90%) in the involved artery (p less than 0.01). Mortality in the acute phase and long-term survival at 4 years (Kaplan-Meier) in patients with nontransmural MI (94%) were similar to those in patients with transmural MI (90%). The occurrence of new nonfatal coronary events was also similar in both groups of MI survivors. Thus, in the absence of symptoms, more aggressive management to improve survival does not seem warranted after nontransmural MI.

Adult↗