Polymorphisms C677T and A1298C of MTHFR Gene: Homocysteine Levels and Prothrombotic Biomarkers in Coronary and Pulmonary Thromboembolic Disease.

The activity of the enzyme methylenetetrahydrofolate reductase (MTHFR) determines homocysteine (Hcy) levels, and polymorphisms in its gene affect the activity of the enzyme. Changes in the enzyme's activity may lead to a higher susceptibility to develop arterial and venous thromboembolic disease. The aim was to analyze the relationship between the C677T and A1298C polymorphisms of MTHFR, Hcy levels, and prothrombotic biomarkers in pulmonary embolism (PE) and acute myocardial ischemia (AMI).

Prevalence of Congenital Heart Disease and Pulmonary Hypertension in Down's Syndrome: An Echocardiographic Study.

Background: Down's syndrome (DS) is a genetic anomaly, which undergoes increased morbidity and mortality when associated with congenital heart disease (CHD). The aims of the study were to determine the prevalence of CHD and pulmonary hypertension (PH) in DS.

Methods: One hundred twenty-seven patients with DS living in Mexico City were evaluated by physical exam, electrocardiogram and echocardiogram.

Left atrial cardiac myxoma. Two unusual cases studied by 3D echocardiography.

We describe two patients with cardiac tumors in the left atrium, which by their association and histopathological lineage, are extremely rare. The clinical, echocardiographic and pathological findings were analysed. The first case was asymptomatic, but in the control studies of colon adenocarcinoma, an intracardiac mass was found by chest computed tomography (CT).

Primary reperfusion in acute right ventricular infarction: An observational study.

Aim: To investigate the impact of primary reperfusion therapy (RT) on early and late mortality in acute right ventricular infarction (RVI).

Methods: RVI patients (n = 679) were prospectively classified as without right ventricular failure (RVF) (class A, n = 425, 64%), with RVF (class B, n = 158, 24%) or with cardiogenic shock (CS) (class C, n = 96, 12%). Of the 679 patients, 148 (21.

The role of pulmonary pressure/cardiac index to identify pulmonary hemodynamic responders to acute oxygen breathing pulmonary hypertension COPD patients.

Objectives: We sought to analyze exercise-derived mean pulmonary artery pressure (Mpap) - cardiac index (CI) - relationship to expand the concepts regarding its nature and to better identify pulmonary hemodynamic responders to acute oxygen breathing (AOB - 99.5%) in pulmonary hypertension (PH) - COPD patients.

Methods: mPAP/CI and extrapolated pressure (Pext) to zero flow were obtained breathing room air (BRA) and under AOB - 99.

Left and right ventricular power: outputs are the strongest hemodynamic correlates to allow identification of acute responders to vasodilator treatment in idiopathic pulmonary arterial hypertension.

Introduction: Despite the prognostic importance of traditionally derived measurements, the significance of right heart catheterization (RHC) remains controversial. Thus, a continued search for hemodynamic markers that define better responsive patients is required. Since, right ventricular failure is the most fatal pathway, right (RVPO) and left (LVPO) ventricular power output are parameters that could provide input for a better understanding of the hemodynamics involved in idiopathic pulmonary artery hypertension (IPAH).

[Pressure-flow relationships interpretation in idiopathic pulmonary arterial hypertension].

Objectives: We analyze exercise-derived mean pulmonary artery pressure/cardiac index relationship to expand the concepts regarding its nature and to better identify "responders" in idiopathic pulmonary arterial hypertension patients.

Methods: Mean pulmonary artery pressure/cardiac index relationship and extrapolated pressure to zero flow were obtained in 40 patients' breathing room air, oxygen 99.5% and hydralazine.

[Clinical interpretation for the pressure-flow relationships in extrinsic allergic alveolitis and in interstitial lung disease pulmonary hypertension patients. Should we care for the lung, the pulmonary artery pressure or both?].

Objectives: We sought to analyze exercise-derived mean pulmonary artery pressure (mPAP)-cardiac index (CI) relationship to expand the concepts regarding its nature and to better identify pulmonary hemodynamic responders to acute oxygen breathing (AO2B-99.5%) and to hydralazine (H) in extrinsic allergic alveolitis (EAA) and chronic interstitial lung disease (CILD) pulmonary hypertension (PH) patients.

Material And Methods: mPAP/CI and extrapolated pressure (Pext) to zero flow were obtained while breathing room air (BRA) and under AO2B-99.

A proposed functional clinical classification predicts in-hospital and long-term survival in the setting of acute right ventricular infarction.

Background: The objectives of the present investigation were to validate the prognostic role of a proposed Clinical Classification [CC], to evaluate the TIMI risk score [RS] and to establish whether the TIMI-RS should incorporate points for patients with acute right ventricular infarction [TIMI-RS-RVI].

Methods And Results: A total of 523 RVI patients were classified on clinical and functional basis as: A, without right ventricular failure [RVF], B with RVF and C with cardiogenic shock. The CC was evaluated prospectively among 98 patients with RVI and retrospectively in 425 RVI patients.

[Staging imagenology in coronary syndromes].

For the physician, it should stand out very clearly that the clinical and rationale analysis of the symptoms observed in every patient suffering from stable chronic ischemic cardiopathy (SCIC) or acute coronary ischemic syndrome (ACIS), are the starting point to apply the available resources in imagenology, in order to apply in an optimized and sequential manner to stratify, without forgetting its inherent limitations, or identify its risk. This approach may be based on the ethics, with special emphasis on the patient economy, which may promote the use of indissoluble medical principles regarding never damaging, but improving, the survival. SCIC and ACIS prevalence is still very high in its actually recognized clinical-pathological avenues.

[Clinical-hemodynamic correlation of the NYHA/WHO system in idiopathic pulmonary artery hypertension. Clinical, therapeutic and long-term prognosis implications].

Background: The most often used functional classification for categorizing the degree of cardiac disability in patients with chronic left ventricular failure is the NYHAN/WHO system. In Idiopathic Pulmonary Arterial Hypertension [I-PAH], this system although used, has not been studied in detail regarding pulmonary hemodynamic parameters association and for long-term prognosis in each of the NYHA/WHO classes.

Methods: We retrospectively, studied the NYHA/ WHO system in 83 I-PAH patients.

[Calculated pulmonary vascular resistance, is definitively a worthless variable. Current methods for a better definition].

The term pulmonary vascular resistance [PVR] describes, in part, the forces opposing the flow across the pulmonary vascular bed. The equation traditionally used is based on the assumption that the pulmonary capillaries, as well as some others vessels in series behave like a Poiseuille resistance. This assumption implies a laminar type of flow of a homogeneous Newtonian fluid, however blood is not a Newtonian fluid and flow is pulsatile in the pulmonary circulation.

[Homeometric autoregulation in the heart. The Anrep effect. Its possible role in increased right ventricular afterload pathophysiology].

One type of intrinsic response exhibited by the isolated and non-isolated heart is the well-known Frank-Starling mechanism, which endows the ventricles with performance characteristics such that the heart ejects whatever volume is put into it [heterometric autoregulation]. A second type of autoregulation in the isolated and no-isolated heart, one which apparently does not utilize the Frank-Starling mechanism, will be the main subject of this review. It requires at least a few beats to develop fully after an increase in activity.

[Reperfusion and postconditioning in acute ST segment elevation myocardial infarction. A new paradigm for the treatment of acute myocardial infarction. From bench to bedside?].

After prolonged periods of ischemia and energy depletion, the ischemic myocardial cell can be jeopardized by specific causes within the reperfusion period. These causes can be viewed as unwanted aspects of the recovery process itself limiting its efficiency. Three potential initial causes of immediate reperfusion injury, aside from oxygen radicals, have been experimentally investigated in detail, and are briefly discussed: 1.

[Clinical stratification of cardiogenic shock].

Cardiogenic shock (CHC) associated to acute myocardial infarct has high mortality and their manifestations are heterogenous. In our institution historical mortality, was 98%, but with different methods of reperfusion, its reduced to 53%. In other hand, with opportune clinical stratification is useful to improve the treatment strategy.

[From the single vulnerable plaque, to the multiple complex coronary plaques. From their basis, to the modern therapeutic approach. A clinical reality in the spectrum of the acute coronary syndromes].

Contemporary clinical and laboratory data have challenged our classical concepts of the pathogenesis of the acute coronary syndromes [ACS]. Indeed, several independent lines of clinical evidence have supported that the critical stenoses cause only a fraction of the ACS. Acute myocardial infarction is believed to be caused by rupture of a vulnerable coronary-artery plaque that appears as a single lesion on angiography.

[The possible clinical role of the cardiac pulmonary power in patients with primary pulmonary hypertension. Initial observations].

The heart is a muscular mechanical pump with an ability to generate both flow [cardiac output] and pressure in the systemic circulation as well in the pulmonary vascular bed. The product of flow output and systemic arterial pressure is the rate of useful work done, or cardiac power output [CP], therefore for the right ventricle and the pulmonary arterial vascular bed it will be: the product of flow output and mean pulmonary arterial pressure will be the rate of useful work done, or cardiac pulmonary power output [CPP]. Cardiac pulmonary pumping reserve capability can be defined as the maximal cardiac pulmonary power output [CPP] achieved by the right heart during maximal stimulation.

[From the single vulnerable plaque, to the multiple complex coronary plaques. From their basis, to the modern therapeutic approach. A clinical reality in the spectrum of the acute coronary syndromes].

Contemporary clinical and laboratory data have challenged our classical concepts of the pathogenesis of the acute coronary syndromes [ACS]. Indeed, several independent lines of clinical evidence have supported that the critical stenoses cause only a fraction of the ACS. Acute myocardial infarction is believed to be caused by rupture of a vulnerable coronary-artery plaque that appears as a single lesion on angiography.

["Cardiac power output" an old tool, possibly a modern tool for assessing cardiac pumping capability, as well as for a short-term prognosis in cardiogenic shock due to acute myocardial infarction].

Hemodynamic monitoring has been used extensively during the last decades for risk stratification and guiding treatment of patients with cardiovascular destabilization, especially in the scenario of acute heart failure and cardiac shock. Every cardiac pump has its own maximum performance, which denotes its pumping capability. The heart is a muscular mechanical pump with an ability to generate both flow (cardiac output) and pressure.

Long-term follow-up of intramyocardial dissecting hematomas complicating acute myocardial infarction.

Intramyocardial dissecting hematoma is a form of subacute cardiac rupture complicating acute myocardial infarction. Initially contained within the myocardial wall, the hematoma may expand, rupture into adjacent structures, or spontaneously resolve. However, long-term follow-up is unknown because clinical and serial imaging data are lacking.

[Mortality in cardiogenic shock].

Objective: Cardiogenic shock (CS) is one of principal causes of mortality after an acute myocardial infarction (MI). The objective of this study was to determine the principal causes that contribute to an increase in mortality in CS.

Methods: We studied 155 consecutive patients with CS admitted to the Coronary Care Unit of the Instituto Nacional de Cardiologia Ignacio Chávez from 1990-2002.

Risk factors, echocardiographic patterns, and outcomes in patients with acute ventricular septal rupture during myocardial infarction.

Ventricular septal rupture (VSR), which can complicate an acute myocardial infarction (MI), carries a high mortality rate. Because precordial and transesophageal echocardiography can identify the type of rupture and assess right ventricular (RV) function at the patient's bedside, we examined the prognostic significance of echocardiographic patterns in postinfarct VSR by postulating that complex rupture and RV involvement carry a worse prognosis. Seventeen patients (10 men; mean age 66 years) who had confirmed postinfarct VSR underwent precordial and transesophageal echocardiography followed by coronary angiography.