The Canadian journal of cardiology
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In early stage uncomplicated systemic hypertension (HT), increased pulmonary vascular resistance (PVR) has been reported at rest, but more rarely during exercise. Recently, limits of normal for stress echocardiography in the evaluation of the pulmonary circulation have been better defined. We therefore used this approach to assess the pulmonary circulation in early HT. ⋯ Resting and exercise PVR are increased in uncomplicated HT, without this being related to increased pulmonary venous pressure or resistive vessel stiffness, suggesting an early increase in pulmonary vascular tone.
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Pulmonary arterial hypertension (PAH) is an obstructive pulmonary vasculopathy, characterized by excess proliferation, apoptosis resistance, inflammation, fibrosis, and vasoconstriction. Although PAH therapies target some of these vascular abnormalities (primarily vasoconstriction), most do not directly benefit the right ventricle (RV). This is suboptimal because a patient's functional state and prognosis are largely determined by the success of the adaptation of the RV to the increased afterload. ⋯ Some molecular pathways, such as those regulating angiogenesis, metabolism, and mitochondrial dynamics, are similarly deranged in the RV and pulmonary vasculature, offering the possibility of therapies that treat the RV and pulmonary circulation. An important paradigm in PAH is that the RV and pulmonary circulation constitute a unified cardiopulmonary unit. Clinical trials of PAH pharmacotherapies should assess both components of the cardiopulmonary unit.
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We aimed to determine the prevalence of iatrogenic aortic dissection in chronic total occlusion (CTO) recanalization procedures, and to assess the management strategy and outcome of such a complication. ⋯ CTO recanalization procedures might be associated with a greater incidence of iatrogenic aortic dissection than non-CTO PCI. The therapeutic strategy and outcome depend on the rapidity of the entry point sealing and the degree of extension of the dissection into the aorta in serial imaging assessment.
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Cardiac troponin is elevated in several clinical settings apart from thrombotic acute coronary syndrome (ACS) and is associated with increased adverse events. It is not clear whether troponin elevation in type II myocardial infarction (MI) is associated with increased cardiovascular events. Our objectives were to identify the cause of mortality in type II MI and to attempt to establish the threshold range of cardiac troponin-I (cTnI) elevation as well as clinical factors associated with adverse outcomes in type II MI. ⋯ Unlike the published literature, our study includes a variety of both operative and nonoperative clinical settings associated with troponin elevation. We illustrate that although overall mortality is high after type II MI, the majority of mortality is caused by noncardiovascular events.