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Biomedical subjects

Ana Clara Tude Rodrigues

Publications and source records attributed to Ana Clara Tude Rodrigues.

6 recordsLinked to original sources

Left ventricular function after exercise training in young men.

The effects of endurance training have been extensively studied in athletes, but longitudinal studies of exercise-induced cardiac changes in normal patients are limited. To assess the effects of 6 months of moderate-intensity aerobic training (1 hour/day, 3 times/week) on normal hearts, 23 sedentary men aged 31.1 +/- 3.5 years were studied by standard and tissue Doppler echocardiography. Left ventricular (LV) systolic function was assessed by the ejection fraction and Doppler-measured stroke volume, and diastolic function was assessed by transmitral and pulmonary venous flow. Tissue Doppler systolic (Sm), early (Em), and late (Am) myocardial velocities were obtained at the septal and lateral mitral annulus. After training, there was a 14.5% increase in peak oxygen consumption (p = 0.000002) and a decrease in heart rate (60 +/- 7 to 56 +/- 8 beats/min, p = 0.01). Septal and posterior wall thickness increased (8.7 +/- 1.0 to 9.4 +/- 1.3 mm, p = 0.002, and 8.2 +/- 0.7 to 8.8 +/- 1.1 mm, p = 0.0009, respectively), with a 15% increase in LV mass index (p = 0.0002). LV diameters, stroke volumes, and ejection fractions were unchanged. Mitral inflow showed a decrease in late-wave velocity (p = 0.00004), thus increasing the early (E)/A ratio. Septal and lateral Sm (p = 0.02) and Em velocities (p <0.05) increased after training. In conclusion, the physiologic increase in LV mass in response to regular exercise in healthy young men occurs in parallel with a decrease in atrial contribution to flow. LV function estimated by tissue Doppler is improved despite the lack of changes in standard echocardiographic indexes.

Adult↗

Left ventricular free wall impeding rupture in post-myocardial infarction period diagnosed by myocardial contrast echocardiography: case report.

BACKGROUND: Left ventricular free wall rupture occurs in up to 10% of the in-hospital deaths following myocardial infarction. It is mainly associated with posterolateral myocardial infarction and its antemortem diagnosis is rarely made. Contrast echocardiography has been increasingly used for the evaluation of myocardial perfusion in patients with acute myocardial infarction, with important prognostic implications. In this case, we reported its use for the detection of a mechanical complication following myocardial infarction. CASE PRESENTATION: A 50-year-old man with acute myocardial infarction in the lateral wall underwent myocardial contrast echocardiography for the evaluation of myocardial perfusion in the third day post-infarction. A perfusion defect was detected in lateral and inferior walls as well as the presence of contrast extrusion from the left ventricular cavity into the myocardium, forming a serpiginous duct extending from the endocardium to the epicardial region of the lateral wall, without communication with the pericardial space. Magnetic resonance imaging confirmed the diagnosis of impending rupture of the left ventricular free wall. While waiting for cardiac surgery, patient presented with cardiogenic shock and died. Anatomopathological findings were consistent with acute myocardial infarction in the lateral wall and a left ventricular free wall rupture at the infarct site. CONCLUSION: This case illustrates the early diagnosis of left ventricular free wall rupture by contrast echocardiography. Due to its ability to be performed at bedside this modality of imaging has the potential to identify this catastrophic condition in patients with acute myocardial infarction and help to treat these patients with emergent surgery.

Echocardiography↗

Intrapericardial echocardiography: a novel catheter-based approach to cardiac imaging.

BACKGROUND: Transvascular catheter-based intracardiac echocardiography has been successfully used to help guide catheter ablation and electrophysiologic procedures. It has recently been demonstrated that catheters can be safely placed into the pericardial space to allow for epicardial cardiac mapping and ablation. We evaluated the feasibility of catheter-based intrapericardial echocardiography (IPE) during such procedures to identify cardiac structures and visualize intracardiac catheters. METHODS: IPE was performed in 7 goats by placing a phased-array ultrasound transducer contained within a 10F steerable catheter into the pericardial space using the same transthoracic subxyphoid approach as used to map and ablate epicardial ventricular tachycardia. Images were obtained of cardiac structures and of intracardiac ablation catheters. After the procedure, the hearts were harvested to assess for possible IPE-related lesions. RESULTS: The IPE catheter could be easily placed inside the pericardial space in all animals. In 7 of 7 cases, longitudinal and short-axis views of right- and left-sided chambers and valves were obtained, similar in orientation to transesophageal echocardiography. Visualization of atrial appendages (6/7), pulmonary veins (6/7), coronary arteries (6/7), and coronary sinus (3/6) was also feasible. Assessment of intracardiac transvalvar and venous blood flow was achieved by spectral and color Doppler. The ablation catheter could be clearly visualized inside cardiac chambers. No arrhythmias were induced with IPE catheter manipulation. After harvesting the hearts, no lesions resulting from the procedure were observed. CONCLUSION: In this experimental setting, IPE was able to provide detailed images of cardiac structures and establish the relative position of the ablation catheter.

Animals↗

Relationship of systolic dysfunction to area at risk and infarction size after ischemia-reperfusion in mice.

Whereas the extent of wall-motion abnormality (WMA) correlates well with the area at risk (AAR) and infarction size in murine models of nonreperfused myocardial infarction, this relationship is less clear in the setting of ischemia-reperfusion injury. Echocardiography was performed in mice at baseline, after left anterior descending coronary artery ligation (30 minutes) followed by reperfusion (24 hours), and after religation of the left anterior descending coronary artery. The extent of WMA before and after religation was compared with the initial infarction size measured by triphenyltetrazolium chloride and the AAR measured by fluorescent microspheres, respectively. Echocardiography showed left ventricular dilation and dysfunction after ischemia and reperfusion. WMA after religation correlated well with AAR (r2 = 0.70, P <.0001). The correlation between WMA and infarction size was incomplete (r2 = 0.59, P <.0002) in part because of underestimation of nontransmural infarcts. Echocardiography can reliably assess AAR after ischemia-reperfusion in mice; however, it does not allow for precise quantification of the small areas of necrosis that often occur in this setting.

Animals↗

A selective inducible NOS dimerization inhibitor prevents systemic, cardiac, and pulmonary hemodynamic dysfunction in endotoxemic mice.

Increased nitric oxide (NO) production by inducible NO synthase (NOS2), an obligate homodimer, is implicated in the cardiovascular sequelae of sepsis. We tested the ability of a highly selective NOS2 dimerization inhibitor (BBS-2) to prevent endotoxin-induced systemic hypotension, myocardial dysfunction, and impaired hypoxic pulmonary vasoconstriction (HPV) in mice. Mice were challenged with Escherichia coli endotoxin before treatment with BBS-2 or vehicle. Systemic blood pressure was measured before and 4 and 7 h after endotoxin challenge, and echocardiographic parameters of myocardial function were measured before and 7 h after endotoxin challenge. The pulmonary vasoconstrictor response to left mainstem bronchus occlusion, which is a measure of HPV, was studied 22 h after endotoxin challenge. BBS-2 treatment alone did not alter baseline hemodynamics. BBS-2 treatment blocked NOS2 dimerization and completely inhibited the endotoxin-induced increase of plasma nitrate and nitrite levels. Treatment with BBS-2 after endotoxin administration prevented systemic hypotension and attenuated myocardial dysfunction. BBS-2 also prevented endotoxin-induced impairment of HPV. In contrast, treatment with NG-nitro-l-arginine methyl ester, which is an inhibitor of all three NOS isoforms, prevented the systemic hypotension but further aggravated the myocardial dysfunction associated with endotoxin challenge. Treatment with BBS-2 prevented endotoxin from causing key features of cardiovascular dysfunction in endotoxemic mice. Selective inhibition of NOS2 dimerization with BBS-2, while sparing the activities of other NOS isoforms, may prove to be a useful treatment strategy in sepsis.

Animals↗

Lung neoplasm mimicking an acute lateral myocardial infarction.

Involvement of the heart and pericardium by cancer is not uncommon, with metastases being more frequent than primary cardiac neoplasms. We present a case of a metastatic lung cancer for which the primary manifestation was chest pain mimicking an acute myocardial infarction.

Aorta↗