RESUMEN

A 54-year-old man, ex smoker with high blood pressure and a history of possible Wolff-Parkinson-White syndrome was admitted for presenting an episode suggestive of acute coronary syndrome with immediate syncope and left bundle branch block, while performing physical activity. Angioplasty and a drug-eluting stent were performed in the left circumflex artery. Subsequently, Doppler echocardiography disclosed an image suggestive of a subaortic membrane. Given these findings, the patient underwent a 3D transesophageal echocardiogram and a magnetic resonance study, which confirmed the diagnosis of a subaortic membrane. In turn, in the Holter monitoring a paroxysmal pattern of Wolff-ParkinsonWhite was observed. The patient presented three possible causes of syncope. A stress echocardiogram elicited a gradient of 126 mm Hg, which could be possibly related to the syncopal episode that the patient suffered.

Paciente masculino de 54 años, ex fumador, hipertenso y con el antecedente no confirmado de síndrome de Wolff-Parkinson-White, que ingresó por haber presentado, mientras realizaba actividad física, un cuadro sugestivo de síndrome coronario agudo con inmediato episodio de síncope y bloqueo de rama izquierda, por lo que se le realizó una angiografía coronaria con posterior angioplastia y la colocación de un stent liberador de drogas en la arteria circunfleja. En el ecocardiograma Doppler se observó una imagen compatible con membrana subaórtica. Ante estos hallazgos se realizó un ecocardiograma transesofágico 3D y una resonancia magnética cardiaca que confirmaron el diagnóstico. A su vez se evidenció en el monitoreo Holter y de forma paroxística el patrón de Wolff-Parkinson-White. De esta manera, el paciente presentó tres posibles causas de síncope. Se realizó un ecocardiograma de esfuerzo, en el que el gradiente intraesfuerzo alcanzó los 126 mm Hg, lo que podría justificar el episodio del síncope.

Asunto(s)

RESUMEN

A 29-year-old man with a history of seizures, was admitted due to an episode of unconsciousness recovered and hypertension with renal disfunction. The electrocardiogram mimicked a hypertrophic cardiomyopathy, but, by Doppler echocardiography, this was discarded because it suggested endomyocardial fibrosis which was confirmed by cardiac magnetic resonance imaging with late enhancement. Since the episode of unconsciousness, brain imaging studies were performed showing vascular sequelae and microangiopathic lesions. These vascular lesions asocciated with renal disfunction with proteinuria within nephrotic range, intensified the search for the etiology arriving to the diagnosis of antiphospholipid syndrome. The patient was discharged with antihypertensive therapy, acenocoumarol, antiepileptic and immunosuppressive drugs.

Paciente masculino de 29 años con antecedentes de convulsiones que ingresa por episodio de pérdida de conocimiento recuperado e hipertensión arterial con deterioro de la función renal. El electrocardiograma simulaba una miocardiopatía hipertrófica que se descartó por ecocardiografía Doppler ya que sugirió una fibrosis endomiocárdica que se confirmó por resonancia magnética nuclear cardíaca con realce tardío. Dado el episodio de pérdida de conocimiento, se realizaron estudios de imágenes cerebrales que mostraban lesiones secuelares vasculares y microangiopáticas. Esto, sumado a la alteración de la función renal con proteinuria en rango nefrótico, intensificó la búsqueda de la causa etiológica y se llegó al diagnóstico de síndrome antifosfolipídico. El paciente fue dado de alta con tratamiento antihipertensivo, acenocumarol, anticonvulsivantes e inmunosupresores.

Asunto(s)

RESUMEN

en

es

RESUMEN

Introducción La ateromatosis carotídea es una alteración temprana de la aterosclerosis subclínica que puede determinarse en forma rápida, económica, repetible y no invasiva. Su correlación anatómica y su asociación con los factores de riesgo y diferentes manifestaciones de aterosclerosis avanzada se han demostrado claramente. En la actualidad, la ateromatosis carotídea se utiliza con frecuencia creciente para caracterizar al paciente con factores de riesgo y para evaluar resultados terapéuticos mediante la determinación del grosor íntima-media carotídeo y de la presencia y el tipo de placas bulbares, ya que se ha demostrado su valor predictivo independiente para eventos isquémicos tanto coronarios como cerebrovasculares. Objetivos Determinar si la presencia y el tipo de placa carotídea (PC) agregan información para predecir futuros eventos cardiovasculares en pacientes de riesgo alto. Material y métodos Se estudiaron 502 pacientes de riesgo alto (múltiples factores de riesgo o antecedente de evento vascular) mediante la determinación del grosor íntima-media máximo (GIMmáx), la presencia (elevación localizada) y el tipo de PC según apariencia ecográfica (fibrocálcica o fibrolipídica), la reactividad humeral dependiente del endotelio (RDE, valor basal arteria humeral vs. a los 5 min de isquemia braquial). Se consideró anormalidad la presencia y el tipo de PC, el GIMmáx > 1,1 mm y la RDE < 5%. Los puntos finales incluyeron la ocurrencia de eventos vasculares o de muerte. Los marcadores de enfermedad vascular se analizaron junto con factores de riesgo (FR) clásicos (edad, diabetes, hipertensión, dislipidemia, tabaquismo y componentes del síndrome metabólico) por el método de riesgos proporcionales de Cox y curvas de Kaplan-Meier. Resultados Edad media 65,5 ± 8,8 años, 354 hombres, 43 eventos durante un seguimiento promedio de 21 meses. Fueron predictores de eventos la PC (RR 5,6; p < 0,001), la dislipidemia (RR 5,5; p < 0,005), el GIMmáx (RR 3,2; p < 0,005), la edad > 65 años (RR 2,7; p < 0,003), la hipertensión sistólica (RR 2,5; p < 0,025), el C-HDL < 50 mg/dl (RR 2,4; p < 0,01), el síndrome metabólico (RR 2,2; p < 0,02), la trigliceridemia > 130 mg/dl (RR 2,1; p < 0,02). Ajustado por los FR, el predictor más potente resultó la PC (RR 3,13; p < 0,05). Los individuos sin PC presentaron un 2,3% de eventos, con PC fibrolipídica un 8,8% y con PC fibrocálcica un 13,4% (p < 0,001). Conclusiones Marcadores de enfermedad vascular temprana, como la presencia y el tipo de PC y el GIMmáx, agregan información pronóstica independiente a los FR. La RDE no agregó información en este grupo. Una metodología simplificada de estudio no invasivo como la empleada puede ser de utilidad clínica en la evaluación del riesgo de eventos vasculares.

Background Carotid atheromatosis is an early manifestation of subclinical atherosclerosis that can be determined in a rapid, economic, repeatable and non-invasive fashion. The anatomic correlation and its association with risk factors and different manifestations of advanced atherosclerosis have been clearly demonstrated. The determination of the intima-media thickness and the presence and type of plaques in the carotid bulb are used to assess carotid atheromatosis in patients with risk factors and to evaluate response to treatment, as this method has an independent predictive value for ischemic coronary and cerebrovascular ischemic events. Objectives To determine whether the presence and type of carotid plaques (CPs) add any information to predict future cardiovascular events in high-risk patients. Material and Methods A total of 502 high-risk patients (with multiple risk factors or history of vascular event) underwent ultrasound evaluation of maximum intima-media thickness (IMTmax), presence (localized protrusion of the vessel wall) and type of (fibrocalcific plaque or fibrolipid plaque) CP, flow mediated dilation of the brachial artery (FMD, brachial artery diameter recorded at baseline and after 5 minutes of brachial ischemia). The following variables were considered abnormal: presence and type of CP, IMTmax >1.1 and FMD <5%. Endpoints included vascular events or mortality. Markers of vascular disease and traditional risk factors (RFs) (age, diabetes, hypertension, dyslipemia, smoking habits and components of the metabolic syndrome) were analyzed together using Cox proportional-hazards regression model and Kaplan-Meier curves. Results Mean age was 65.5±8.8 years and 354 were men; 43 events occurred during an average follow-up of 21 months. The presence of CP (RR 5,6; p <0.001), dyslipemia (RR 5.5; p <0.005), IMTmax (RR 3.2; p <0.005), age > 65 years (RR 2.7; p <0.003), systolic hypertension (RR 2.5; p <0.025), HDL-C <50 mg/dl (RR 2.4; p <0.01), metabolic syndrome (RR 2.2; p <0.02), and triglyceride levels >130 mg/dl (RR 2.1; p <0.02) were predictors of events. After adjusting for RFs, PC was the most powerful predictor (RR 3.13; p <0.05). The incidence of events was 2.3% in the absence of CP, 8.8% with fibrolipid plaque, and 13.4% with fibrocalcific plaque p <0.001). Conclusions The presence and type of CP anf IMTmax are markers of early vascular disease providing prognostic information independent of RFs. FMD did not provide additional information in this group. This simple, non-invasive method may be clinically useful in the evaluation of the risk of vascular events.

RESUMEN

Antecedentes Los agentes inhibidores de la fosfodiesterasa 5, como el sildenafil, son vasodilatadores moderados ampliamente utilizados para el tratamiento de la disfunción eréctil. En la actualidad, la evidencia disponible establece su potencial aplicación en otras patologías, como la hipertensión pulmonar, la disfunción endotelial y la insuficiencia cardíaca crónica. Objetivo El presente estudio fue diseñado para comprobar si la administración de sildenafil en pacientes con insuficiencia cardíaca crónica en clase funcional II-III mejora la capacidad de ejercicio en comparación con placebo. Material y métodos Se seleccionaron en forma aleatoria 70 pacientes portadores de insuficiencia cardíaca crónica de cualquier etiología, excepto valvulares, todos con tratamiento óptimo. Para su inclusión en el estudio, los pacientes debían tener un diámetro diastólico ventricular izquierdo > 55 mm, una fracción de eyección < 35% y una presión arterial sistólica > 90 mm Hg. Se excluyeron los que se encontraban anémicos, aquellos con indicación de cirugía por cualquier causa o los que por diversos motivos no pudieran realizar una caminata de seis minutos. Luego de una caminata de seis minutos fueron aleatorizados para recibir 50 mg de sildenafil o placebo, conformándose dos grupos, placebo y sildenafil, ambos con 35 participantes. Luego de 1 hora de la ingestión de las drogas se realizó una nueva caminata de seis minutos. Antes y después de cada caminata se controlaron las siguientes variables: presión arterial sistólica, diastólica y frecuencia cardíaca; se registraron también los metros caminados en cada prueba. Resultados Características generales, grupo placebo versus grupo sildenafil: hombres: 74% vs 88%, etiología isquémico-necrótica: 71% vs 77%, clase funcional II: 37% vs 34%, clase funcional III: 63% vs 66%, edad: 68 ± 10 vs 68 ± 12 años, fracción de eyección: 26,5% ± 7,8% vs 26,5% ± 6,5%, diámetro diastólico ventricular izquierdo: 65 ± 6 vs 66 ± 9 mm (todas p = ns). Las variables del grupo placebo versus sildenafil antes de la primera caminata fueron: presión arterial sistólica: 115 ± 15 vs 115 ± 21 mm Hg y diastólica: 71 ± 10,5 vs 68 ± 13 mm Hg (ambas p = ns) y frecuencia cardíaca: 74 ± 13 vs 64 ± 6 (p < 0,001). Luego de la primera caminata y antes de la administración de las drogas: presión arterial sistólica: 126 ± 20 vs 133 ± 26 mm Hg, diastólica: 68 ± 11 vs 72 ± 15 mm Hg y frecuencia cardíaca 84 ± 2 vs 80 ± 9 (todas p = ns). Antes de la segunda caminata y luego de la administración de las drogas, grupo placebo versus sildenafil: presión arterial sistólica: 112 ± 14 vs 95 ± 18 mm Hg, diastólica: 69 ± 8 vs 57 ± 12 mm Hg (ambas p < 0,001) y frecuencia cardíaca: 73 ± 11 vs 75 ± 10 (p = ns). Finalmente, luego de la segunda caminata, presión arterial sistólica: 123 ± 17 vs 115 ± 26 mm Hg (p < 0,05), diastólica: 65 ± 7 vs 60 ± 12 mm Hg (p < 0,02) y frecuencia cardíaca: 84 ± 13 vs 86 ± 12 (p = ns). Cuatro pacientes (11%) en el grupo sildenafil presentaron cefalea y ninguno en el grupo placebo. No se registraron eventos mayores. El grupo sildenafil caminó 222 ± 69 metros antes y 313 ± 76 luego de la administración de la droga; la diferencia en metros fue de 91 ± 19. El grupo placebo caminó 233 ± 67 metros antes y 242 ± 67 luego de la administración de la droga; la diferencia en metros fue de 9 ± 5. Al comparar estos resultados, la diferencia en metros recorridos resultó significativa a favor del grupo sildenafil: 91 ± 19 vs 9 ± 5 (p < 0,0001). Conclusiones En pacientes con insuficiencia cardíaca en clase funcional II-III bajo tratamiento óptimo, el sildenafil mejoró la capacidad de ejercicio en comparación con placebo.

Background Phosphodiesterase type 5 inhibitors, as sildenafil, are moderate vasodilators widely used for erectile dysfunction. The evidence currently available establishes that they are potentially useful to treat other conditions like pulmonary hypertension, endothelial dysfunction and chronic heart failure. Objective To evaluate whether sildenafil is useful to improve exercise capacity compared to placebo in patients with chronic heart failure in functional class II-III. Material and Methods A total of 70 patients with chronic heart failure of any etiology, excluding valvular heart disease, were randomly selected. All patients were receiving optimal medical treatment. Patients were included if they had a left ventricular-diastolic diameter of 55 mm, an ejection fraction <35% systolic blood pressure >90 mm Hg. Patients with anemia, an indication of surgery due to any cause, and those unable to undergo a 6-minute walk test were excluded from the study. After the 6-minute walk test, the patients were randomly assigned to receive 50 mg of sildenafil (sildenafil group) or placebo (placebo group); each group had 35 patients. A second 6-minute walk test was performed 1 hour after the drug was administered. The following variables were evaluated before and after each test: systolic blood pressure, heart rate and the distance walked in meters in each test. Results General characteristic, placebo group versus sildenafil group: men: 74% vs. 88%, ischemic dilated cardiomyopathy: 71% vs. 77%, functional class II: 37% vs. 34%, functional class III: 63% vs. 66%, age: 68±10 vs. 68±12 years, ejection fraction: 26.5%±7.8% vs. 26.5%±6.5%, left ventricular end-diastolic diameter: 65±6 vs. 66±9 mm (all p = ns). Before the fírst 6-minute walk test, the following variables were measured in the placebo versus the sildenafil group: systolic blood pressure: 115±15 vs. 115±21 mm Hg; diastolic blood pressure: 71±10.5 vs. 68±13 mm Hg (both p = ns); heart rate: 74±13 vs. 64±6 (p <0.001). After the first test and before drug administration: systolic blood pressure: 126±20 vs. 133±26 mm Hg, diastolic blood pressure: 68±11 vs. 72±15 mm Hg; heart rate 84±2 vs. 80±9 (all p = ns). Before the second test and after drug administration, placebo versus sildenafil: systolic blood pressure: 112±14 vs. 95±18 mm Hg; diastolic blood pressure: 69±8 vs. 57±12 mm Hg (both p <0.001); heart rate: 73±llvs. 75±10 (p = ns). Finally after the second walk test: systolic blood pressure: 123±17 vs. 115±26 mm Hg (p <0.05), diastolic blood pressure: 65±7 vs. 60±12 mm Hg (p <0.02) and heart rate: 84±13 vs. 86±12 (p = ns). The incidence of headache was 11% (4 patients) in the sildenafil group and 0% in the placebo group. No major events were reported. The sildenafil group walked 222±69 and 313±76 meters before and after drug administration, respectively; the difference was 91±19 meters. The placebo group walked 233±67 and 242±67 meters before and after drug administration, respectively; the difference was 9±5 meters. The difference in the distance walked was greater in the sildenafil group: 91±19 vs. 9±5 (p <0.0001). Conclusions In patients with heart failure in functional class II-III under optimal medical therapy, sildenafil improved exercise capacity compared to placebo.

RESUMEN

The endothelium is the common target of all cardiovascular risk factors, and functional impairment of the vascular endothelium in response to injury occurs long before the development of visible atherosclerosis. The endothelial cell behaves as a receptor-effector structure which senses different physical or chemical stimuli that occur inside the vessel and, therefore, modifies the vessel shape or releases the necessary products to counteract the effect of the stimulus and maintain homeostasis. The endothelium is capable of producing a large variety of different molecules which act as agonists and antagonists, therefore balancing their effects in opposite directions. When endothelial cells lose their ability to maintain this delicate balance, the conditions are given for the endothelium to be invaded by lipids and leukocytes (monocytes and T lymphocytes). The inflammatory response is incited and fatty streaks appear, the first step in the formation of the atheromatous plaque. If the situation persists, fatty streaks progress and the resultant plaques are exposed to rupture and set the conditions for thrombogenesis and vascular occlusion. Oxidant products are produced as a consequence of normal aerobic metabolism. These molecules are highly reactive with other biological molecules and are referred as reactive oxygen species (ROS). Under normal physiological conditions, ROS production is balanced by an efficient system of antioxidants, molecules that are capable of neutralizing them and thereby preventing oxidant damage. In pathological states, ROS may be present in relative excess. This shift of balance in favor of oxidation, termed 'oxidative stress', may have detrimental effects on cellular and tissue function, and cardiovascular risk factors generate oxidative stress. Both type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetic patients have mostly been described under enhanced oxidative stress, and both conditions are known to be powerful and independent risk factors for coronary heart disease, stroke, and peripheral arterial disease. Hyperglycemia causes glycosylation of proteins and phospholipids, thus increasing intracellular oxidative stress. Nonenzymatic reactive products, glucose-derived Schiff base, and Amadori products form chemically reversible early glycosylation products which subsequently rearrange to form more stable products, some of them long-lived proteins (collagen) which continue undergoing complex series of chemical rearrangements to form advanced glycosylation end products (AGEs). Once formed, AGEs are stable and virtually irreversible. AGEs generate ROS with consequent increased vessel oxidative damage and atherogenesis. The impressive correlation between coronary artery disease and alterations in glucose metabolism has raised the hypothesis that atherosclerosis and diabetes may share common antecedents. Large-vessel atherosclerosis can precede the development of diabetes, suggesting that rather than atherosclerosis being a complication of diabetes, both conditions may share genetic and environmental antecedents, a 'common soil'.

Asunto(s)

RESUMEN

The endothelium is a thin monocellular layer that covers all the inner surface of the blood vessels, separating the circulating blood from the tissues. It is not an inactive organ, quite the opposite. It works as a receptor-efector organ and responds to each physical or chemical stimulus with the release of the correct substance with which it may maintain vasomotor balance and vascular-tissue homeostasis. It has the property of producing, independently, both agonistic and antagonistic substances that help to keep homeostasis and its function is not only autocrine, but also paracrine and endocrine. In this way it modulates the vascular smooth muscle cells producing relaxation or contraction, and therefore vasodilatation or vasoconstriction. The endothelium regulating homeostasis by controlling the production of prothrombotic and antithrombotic components, and fibrynolitics and antifibrynolitics. Also intervenes in cell proliferation and migration, in leukocyte adhesion and activation and in immunological and inflammatory processes. Cardiovascular risk factors cause oxidative stress that alters the endothelial cells capacity and leads to the so called endothelial "dysfunction" reducing its capacity to maintain homeostasis and leads to the development of pathological inflammatory processes and vascular disease. There are different techniques to evaluate the endothelium functional capacity, that depend on the amount of NO produced and the vasodilatation effect. The percentage of vasodilatation with respect to the basal value represents the endothelial functional capacity. Taking into account that shear stress is one of the most important stimulants for the synthesis and release of NO, the non-invasive technique most often used is the transient flow-modulate "endothelium-dependent" post-ischemic vasodilatation, performed on conductance arteries such as the brachial, radial or femoral arteries. This vasodilatation is compared with the vasodilatation produced by drugs that are NO donors, such as nitroglycerine, called "endothelium independent". The vasodilatation is quantified by measuring the arterial diameter with high resolution ultrasonography. Laser-Doppler techniques are now starting to be used that also consider tissue perfusion. There is so much proof about endothelial dysfunction that it is reasonable to believe that there is diagnostic and prognostic value in its evaluation for the late outcome. There is no doubt that endothelial dysfunction contributes to the initiation and progression of atherosclerotic disease and could be considered an independent vascular risk factor. Although prolonged randomized clinical trials are needed for unequivocal evidence, the data already obtained allows the methods of evaluation of endothelial dysfunction to be considered useful in clinical practice and have overcome the experimental step, being non-invasive increases its value making it use full for follow-up of the progression of the disease and the effects of different treatments.

Asunto(s)

Asunto(s)

Asunto(s)

RESUMEN

Assessment of the left ventricular mass (LVM) from electrocardiograms may be improved by the addition of clinical variables into a multivariate equation. As the heart-thorax distance may affect the results, its relationships with electrocardiographic and clinical data have been evaluated in a group of 220 subjects (53 +/- 15 years, 126 female, 175 without demonstrated heart disease) who were assessed for echocardiographic LVM and heart-thorax distance. Sokolow, Cornell, and total QRS voltage indexes were obtained. Multiple regression equations with LVM as the dependent variable were fit, with an ECG index, body mass index (BMI), age, and gender as the independent predictors. Each of the 3 ECG indexes, BMI, age, and sex was shown to be independent predictors of LVM, with the ECG and BMI contributing with most of the explanatory power. When added to the model, the distance from the interventricular septum to the precordium (septal-LVD) was not a predictor of LVM, but when BMI was withdrawn, septal-LVD became an independent predictor of LVM (P < .001). This was not observed when septal-LVD was substituted for any other clinical or ECG variable, thus suggesting that septal-LVD accounts for information contained in BMI but not in the remaining variables. In addition, the distance from the center of LV to the precordium (mid-LVD) achieved significance as an independent LVM predictor, although the coefficient of multiple determination (R) practically did not change. Almost identical results are obtained when LVM is indexed for body surface area. Body mass index supplies virtually all the information contained in the heart-thorax distance.

Asunto(s)