Efrén Martínez-Quintana

Serum and 24-hour urine analysis in adult cyanotic and noncyanotic congenital heart disease patients.

INTRODUCTION Glomerulopathy is a complication of congenital heart disease patients. The risk of developing renal impairment is particularly high in cyanotic patients. OBJECTIVE The aim of this study was to determine the prevalence of renal dysfunction and microalbumiuria in adult cyanotic and non cyanotic congenital heart disease patients. METHODS Fourteen cyanotic and 22 noncyanotic congenital heart disease patients were studied in the Adult Congenital Heart Disease Unit at the Complejo Hospitalario Universitario Insular-Materno Infantil. Demographic characteristics, complete blood count, and 24-hour urianalysis were obtained, including abdominal ultrasound in those with cyanosis. RESULTS No differences were seen between age (years) (27.4 +/- 8.2; 26.4 +/- 8.3; P = .71), sex, size, weight, or glomerular filtration rate (mL/min/1.73 m(2)) (81.1 +/- 22.9 vs. 84.9 +/- 9.2, P = .482) between cyanotic and noncyanotic patients. However, Eisenmenger patients had significantly impaired renal function when compared with noncyanotic patients (73.0 +/- 17.3 vs. 84.9 +/- 9.2 mL/min/1.73 m(2), P = .023). Significant differences were obtained in oxygen saturation (%) (83.8 +/- 5.8 vs. 97.8 +/- 0.8; P = .000), hematocrit (%) (59.3 +/- 8.1 vs. 40.9 +/- 8.5; P = .000), platelets (10(3)/microL) (161.5 +/- 70.5 vs. 277.9 +/- 57.6; P = .000), serum uric acid (mg/dL) (7.5 +/- 2.3 vs. 5.6 +/- 1.5; P = .008) and microalbuminuria (mg/24 hours) (12.8 [0, 700.2] vs. 2.4 [0, 18.9]; P = .000) between cyanotic and noncyanotic patients. Five cyanotic patients (35.7%) had microalbuminuria (>30 mg/24 hours) and three of them (21.4%) proteinuria (>1 g/24 hours). No significant differences were seen between serum and urine parameters between cyanotic patients who had microalbuminuria (>30 mg/24 hours) and those cyanotic patients who did not have it (<30 mg/24 hours). CONCLUSIONS Renal impairment is frequently seen in congenital heart disease patients, being associated occasionally with proteinuria and microalbuminuria in cyanotic ones.

Serum glucose and lipid levels in adult congenital heart disease patients.

Atherosclerosis has been correlated with known cardiovascular risk factors such as serum glucose or lipid levels. Because congenital heart disease patients tend to survive until adulthood, atherosclerosis has also become a matter of concern in these patients. One hundred fifty-eight congenital heart disease patients and 152 patients selected at random from the population were studied and compared to determine serum glucose, total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein cholesterol, and triglycerides levels. Both groups had similar socioeconomic status levels and the same environmental influences. Significant differences were seen between congenital heart disease patients and the control group, after sex, age, and body mass index adjustment, in fasting plasma glucose (97.7 [94.2-101.2] vs 86.9 [83.2-90.7], P < .001), total cholesterol (171.5 [165.7-177.3] vs 199.8 [90.7-206.0], P < .001), LDL cholesterol (103.9 [98.8-108.8] vs 123.8 [118.5-129.1], P < .001), and high-density lipoprotein cholesterol (48.1 [46.2-50.0] vs 54.2 [52.1-56.2], P < .001) levels. Nonsignificant differences were seen in triglycerides concentrations. Those patients with ventricular septal defect, coarctation of the aorta, and cyanosis had the lowest total cholesterol and LDL cholesterol concentrations. Congenital heart disease patients have lower plasma cholesterol concentrations and higher serum glucose levels than noncongenital ones.

Cor Triatriatum Dexter versus Prominent Eustachian Valve in an Adult Congenital Heart Disease Patient

An eustachian valve (EV) remnant, if present, is usually noted by the presence of a thin ridge or a crescent-shaped fold of endocardium arising from the anterior rim of the inferior vena cava orifice due to the persistence of the right sinus venosus valve. Though the embryologic explanation of cor triatriatum dexter (CTD) is the same as that of the normal formation of the EV--lack of regression of the right sinus venosus valve--it is usually called CTD or divided right atrium when there are attachments on the atrial septum giving the appearance of a divided atrium. However, its called prominent eustachian valve when the right sinus venosus valve has partly regressed, with no remaining septal attachments and without the appearance of a divided atrium. We present the case of an adult patient with an atrial septal defect with a high insertion of a giant EV, which mimics the echocardiographic appearance of divided right atrium.

Androgenic Anabolic Steroid, Cocaine and Amphetamine Abuse and Adverse Cardiovascular Effects

Introduction: Anabolic-androgenic steroids (AAS), a synthetic derivate of testosterone, have become a popular drug among athletes and bodybuilders to enhance muscle mass and improve the athletic performance. Many pathological effects such as hepatic and endocrine dysfunction, behavioural changes and cardiovascular complications have been reported. Case Report: Within these ast ones, we find an increase in left ventricular muscle mass, concentric myocardial hypertrophy, left ventricular diastolic dysfunction, arterial hypertension, prothrombotic effects, changes in the concentration of cholesterol levels, particularly a reduction in HDL cholesterol concentration, myocardial infarctions in relation to endothelial dysfunction, vasospasms or thrombosis and sudden cardiac death. Discussion: We report the case of a 32-year-old patient with a history of arterial hypertension, depressive syndrome and consumption of cocaine, amphetamines and AAS who developed severe left ventricular systolic dysfunction and myocardial hypertrophy with signs of heart failure and peripheral arterial embolism.

Iron deficiency anemia detection from hematology parameters in adult congenital heart disease patients.

INTRODUCTION Iron deficiency anemia is the most common single cause of anemia worldwide. The purpose of our study was to estimate the prevalence of anemia in adult congenital heart disease (ACHD) patients, compare different hematology parameters between hypoxemic and nonhypoxemic ACHD patients, and determine which parameters detect iron deficiency anemia in hypoxemic ACHD patients. METHODS ACHD patients were studied and blood samples collected for determination of hemoglobin, derived red cell indices, serum iron, apoferritin, total iron-binding capacity, transferrin saturation index, C-reactive protein (CRP), and N-terminal proB-type natriuretic peptide (NT-proBNP) levels. RESULTS Two hundred seventy-eight ACHD patients, mean age 31.6 ± 14.3 years old, were studied. One hundred sixty-seven (60%) patients were male. Two hundred forty-five patients were nonhypoxemic and 33 patients were hypoxemic. Hypoxemic ACHD patients had significant higher hemoglobin concentration (g/dL) (17.5 ± 3.5 vs. 14.6 ± 1.7, P <.001), red cell distribution width (RDW) (%) (17.0 ± 3.3 vs. 14.1 ± 7.6, P <.034), apoferritin (ng/mL) (19.8 [4.1-147.2] vs. 38.0 [6.7-191.2], P =.019), CRP (mg/dL) (0.50 [0.0-3.8] vs. 0.12 [0.0-1.4], P <.001), and NT-proBNP (pg/mL) (409.3 [33.3-9830.8] vs. 5.2 [0.0-1068.4], P <.001) levels than nonhypoxemic ACHD patients. Serum iron, total iron-binding capacity, and transferrin saturation index were not statistically significant between hypoxemic and nonhypoxemic ACHD patients. In the hypoxemic group, 15 (45%) patients had apoferritin levels <20 ng/mL and eight (24%) patients developed microcytosis and hypochromia. A RDW above the normal range (>14.5%) in hypoxemic ACHD patients allowed the detection of an apoferritin level <20 ng/mL with a sensitivity of 93%. CONCLUSIONS RDW seems to be a useful and economic tool to detect low serum apoferritin levels in hypoxemic ACHD patients.

Necrosis miocárdica y disfunción biventricular severa en el contexto de abuso crónico de efedrina

La efedra es un compuesto similar a la anfetamina con un potente efecto simpaticomimetico. La efedrina, su componente activo, es usado ampliamente para reducir peso, mejorar la forma atletica o como componente de algunos farmacos. Los efectos cardiovasculares de la efedrina incluyen taquicardia, aumento de la contractilidad miocardica, vasoconstriccion arterial e hipertension arterial, efectos por los que suele ser usada terapeuticamente. Sin embargo, tambien puede producir efectos adversos tales como neuropatia, miopatia, psicosis, adiccion, accidentes cerebrovasculares, insomnio, miocarditis, arritmias, infarto de miocardio o muerte subita. Presentamos el caso de un paciente con antecedentes psiquiatricos, que desarrollo fallo cardiaco congestivo y edema agudo de pulmon en el contexto de disfuncion biventricular severa y necrosis miocardica secundaria a abuso cronico de efedrina. Otras causas de miocardiopatia dilatada, tales como alcoholismo, autoinmunidad, hemocromatosis, alteraciones tiroideas, miocarditis bacteriana o viral y enfermedad arterial coronaria fueron descartadas. Tras cinco anos de abandono total del farmaco, el paciente se encuentra libre de sintomas con recuperacion parcial de la fraccion de eyeccion ventricular izquierda.

Serum uric acid levels and cardiovascular disease: the Gordian knot

Hyperuricemia is defined as serum uric acid level of more than 7 mg/dL and blood levels of uric acid are causally associated with gout, as implicated by evidence from randomized clinical trials using urate lowering therapies. Uric acid as a cardiovascular risk factor often accompanies metabolic syndrome, hypertension, diabetes, dyslipidemia, chronic renal disease, and obesity. Despite the association of hyperuricemia with cardiovascular risk factors, it has remained controversial as to whether uric acid is an independent predictor of cardiovascular disease. To settle this issue, and in the absence of large randomized controlled trials, Mendelian randomization analysis in which the exposure is defined based on the presence or absence of a specific allele that influences a risk factor of interest have tried to shed light on this.

Thrombocytopenia in congenital heart disease patients

Abstract Thrombocytopenia has been identified as a mechanism of the increased incidence of thromboembolism and death in hypoxemic congenital heart disease (CHD) patients. About 387 CHD patients (344 non-hypoxemic and 43 hypoxemic) were followed-up during a median of 34.3 (24.5; 49.9) months. Demographic, clinical, analytical parameters, and survival curves between CHD with platelet levels above and below 150 000/μl were determined. On one hand, in the subgroup of non-hypoxemic CHD patients, 8 out of 344 (2.3%) patients showed some type of bleeding and 8 (2.3%) patients showed some type of thrombosis. On the other hand, in the hypoxemic subgroup, 6 out of 43 (13.9%) patients had some type of bleeding and 5 (11.6%) patients showed some type of thrombosis. The binary logistic regression multivariate analysis being under oral anticoagulation/antiplatelet therapy (OR, 4.192 (1.207–14.550), p = 0.024) and having hypoxemia (OR, 4.041 (1.087–15.029); p = 0.037) favored the occurrence of bleeding. Meanwhile, the only factor which favored thrombosis was being hypoxemic (OR, 5.703 (1.334–24.387); p = 0.019). Also, being hypoxemic (OR, 0.217 (0.070–0.670), p = 0.008) and having a high MPV (OR, 0.534 (0.383–0.744); p = 0.001) favored a low platelet count (< 150 × 103/µl). Kaplan–Meier survival analysis showed significant differences between CHD patients with a platelet count lower and higher than 150 × 103/μl (p = 0.009). Bleeding and thrombotic complications are more frequent in hypoxemic CHD patients irrespective of platelet counts. Larger platelets, as reflected by an increased mean platelet volume, and the higher CRP concentration seen in hypoxemic CHD patients may explain to some extent the higher incidence of thrombotic events in hypoxemic patients.

Proteinuria and clinical outcome in CHD patients.

INTRODUCTION CHD patients, especially those with associated hypoxaemia, usually have some level of renal function impairment, even though they are relatively young. The aim of the study was to evaluate those clinical and analytical factors that may contribute to microalbuminuria and determine the association of 24-hour proteinuria with thrombotic events and mortality. METHODS A total of 251 CHD patients were studied and demographic characteristics, blood test, and 24-hour urinalysis were analysed. RESULTS Of the patients, 221 were non-hypoxaemic, and 30 were hypoxaemic (oxygen saturation of 84.3±5.9%). Of the non-hypoxaemic patients, 30 (13.6%), and of the hypoxaemic patients 9 (30%), showed proteinuria (>0.15 g/24 hours) (p=0.028). Hypoxaemic CHD patients also showed higher haematocrit (%) (50.7 (34.6; 72.1) versus 42.8 (34.6; 48.9), p<0.001), serum creatinine (mg/dl) (1.07±0.2 versus 0.96±1.9, p=0.004), microalbuminuria (mg/dl/24 hours) (1.2 (0.0; 261.5) versus 0.5 (0.0; 4.37), p<0.001), proteinuria (gr/24 hours) (1.0 (0.4; 3.1) versus 0.08 (0.04; 0.52), p=0.043), and N-terminal pro-B-type natriuretic peptide (pg/ml) (417.8 (35.7; 8534.0) versus 44.9 (0.0; 670.5), p<0.001) concentrations than non-hypoxaemic CHD patients. During a median follow-up of 26.0 (16.9; 57.7) months, five patients died - one patient had 24-hour proteinuria and four patients did not (p=0.581) - and three patients had some type of thrombosis - two patients had 24-hour proteinuria and one patient did not (p=0.014). Kaplan-Meier survival analysis showed no significant difference between CHD patients with and without 24-hour proteinuria (p=0.631). CONCLUSION CHD patients with proteinuria have significantly more thrombosis and more hypoxaemia than those patients without proteinuria.

Positive clinical response to clopidogrel is independent of paraoxonase 1 Q192R and CYP2C19 genetic variants.

There is increasing controversy about the influence of serum paraoxonase type 1 and cytochrome CYP2C19 in the conversion of clopidogrel to its pharmaceutically active metabolite. The effect of concomitant medication with the proton pump inhibitor omeprazole has been also subject of intense scrutiny.