Heart and vessels
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This report describes the case of a patient who developed acute myocardial infarction with ST segment elevation in anterior and inferior leads, simultaneously. After treatment with systemic thrombolysis, and after an initial short-lasting symptomatic improvement, chest pain and ST segment elevation recurred. ⋯ Percutaneous coronary angioplasty and stent implantation were successfully performed at both lesions. This case supports the concept that, at least in some patients, acute coronary artery disease reflects a diffuse pathophysiologic process that may lead to multifocal plaque instability associated with clinical instability at multiple sites.
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Comparative Study
Chlamydia pneumoniae seropositivity predicts the risk of restenosis after percutaneous transluminal coronary angioplasty.
This study was done to evaluate whether anti-Chlamydia pneumoniae seropositivity can be a predictor of restenosis after coronary intervention. Recent studies indicate that latent infection with C. pneumoniae is associated with and could possibly cause atherosclerosis. However, it is unknown whether chronic infection with this microorganism is involved in the mechanism of restenosis after percutaneous transluminal coronary angioplasty. ⋯ Lesions in the seropositive patients had a greater mean loss index (mean +/- SD 0.75 +/- 0.45 vs 0.35 +/- 0.41, P < 0.001), which was defined as late loss (luminal diameter reduction at follow-up angiography) divided by acute gain (luminal diameter gain by angioplasty), in late loss (1.07 +/- 0.64mm vs 0.65 +/- 0.79mm, P = 0.019), in percentage of diameter stenosis (57% +/- 20% vs 41% +/- 21%, P = 0.003) and a lesser mean in minimal luminal diameter (1.18 +/- 0.58 mm vs 1.67 +/- 0.63 mm, P = 0.002) at follow-up angiography. In a multivariate logistic regression model, anti-C. pneumoniae IgG seropositivity was a strong independent predictor of restenosis compared to the other risk factors (odds ratio = 6.2, P = 0.01). C. pneumoniae could play an important role in the mechanism of restenosis and evaluation of the IgG seropositivity, and may help to identify patients at high risk for restenosis.
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Case Reports
Extracorporeal membrane oxygenation and left ventricular assist device: a case of double mechanical bridge.
A 14-year-old boy with dilated cardiomyopathy with cardiac arrest was successfully implanted with a left ventricular assist device (LVAD) after 6-day extracorporeal membrane oxygenation (ECMO). He had multiple organ failure at the initiation of ECMO, but the failed organs recovered during assisted circulation, leading to LVAD implantation. This case showed the advantages of the "double bridge" such as: (1) quick and easy installation for acute cardiogenic shock, (2) providing intervention time for complications refractory to LVAD implantation, and (3) providing evaluation time for potential LVAD implantation and transplant candidates.
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The left ventricular (LV) end-systolic pressure-volume relation (ESPVR) is a load-insensitive method for evaluating LV contractility, which needs invasive measurement. Some noninvasive methods substitute peak aortic pressure (Ps) for end-systolic LV pressure by assuming there is no difference between these pressures. However, this assumption has not been directly validated. ⋯ Ps/V(EE) correlated worst with Ees(LV). Central AOP can be substituted for LVP to derive EesLV. Other estimation methods yield weaker and poor correlations to directly measured Ees.
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Case Reports
Effects of milrinone for right ventricular failure after left ventricular assist device implantation.
Right ventricular failure after left ventricular assist device implantation sometimes requires additional mechanical right ventricular support. The effectiveness of nitrates, prostaglandin, or nitric oxide inhalation in such cases has already been reported. However, there are few reports on the administration of phosphodiesterase inhibitor for right ventricular failure after left ventricular assist device implantation. ⋯ Both had residual pulmonary hypertension due to high pulmonary vascular resistance after left ventricular assist device implantation. However, intravenous milrinone caused a significant reduction in pulmonary vascular resistance and an increase in left ventricular assist device flow. Milrinone acts as both an inotropic agent and a direct vasodilator, and thus may avoid the need for mechanical support for right ventricular failure due to residual pulmonary hypertension after left ventricular assist device implantation.