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Background and Objective: Patients with chronic pulmonary hypertension (CPH) who demonstrate pulmonary vasodilation following calcium-channel blocker (CCB) administration are defined as 'responders'. In contrast, 'nonresponders' are patients who do not show such pulmonary vasodilation with CCB therapy. The purpose of this investigation was to study the effects of CCB therapy on right heart mechanics in experimental CCB responders versus CCB nonresponders.Methods: In 12 dogs, right atrial (RA) and ventricular pressure and volume (conductance catheters) were simultaneously recorded after 3 months of progressive pulmonary artery banding. Diltiazem was given at 10 mg h with the pulmonary artery constricted (simulated CCB nonresponder). Responders were then created by releasing the pulmonary artery band to unload the ventricle. RA and right ventricular contractility and diastolic stiffness (slope of end-systolic and end-diastolic pressure-volume relations) were calculated and RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed compared with open, respectively.Results: With CCB, RA contractility (P < 0.03) and cardiac output (P < 0.004) were compromised in simulated nonresponders whereas RA stroke work was pharmacologically depressed in the setting of an unchanged afterload. After simulating a responder by controlled pulmonary artery band release, the right atrium became less distensible, causing a shift from reservoir to conduit function (P < 0.001) towards physiological baseline conditions and a recovery in the hyperdynamic compensatory response in both chambers (P < 0.007) as evidenced by declined RA and right ventricular contractility with an improved cardiac output as compared with CPH and simulated nonresponders. RA and right ventricular diastolic function in both groups was not affected by CCB.Conclusion: CCB did not affect right ventricular function in simulated nonresponders but significantly impaired RA contractility and cardiac output. In simulated responders, afterload fell substantially, thereby allowing the right atrium and right ventricle to recover from their pathological hyperdynamic contractile response to CPH. This effect outweighed the intrinsic negative effects of CCB therapy on systolic RA function. Current data suggest that the right atrium in CPH is much more sensitive to CCB therapy than the right ventricle and show for the first time why CCB therapy in CPH has been empirically restricted to documented responders. [ABSTRACT FROM AUTHOR]

Acute arterial disruptions of the thoracic aorta are rare and often lethal. They are most often due to blunt trauma and occur most commonly just distal to the left subclavian artery origin in the setting of multisystem injuries. The very proximal nature of the lesion in survivors makes open surgical repair hazardous, with mortality rates reaching over 20%. Endovascular therapy is a new and attractive option for the treatment of those challenging patients. Since March 2002, 3 patients with blunt and 1 patient with a stable iatrogenic descending aortic injury were successfully treated at this institution. Spiral computed tomography followed by angiography was used for diagnosis. No preexisting aortic pathology was present. Major associated injuries included unstable thoracic spinal fractures, abdominal solid organ injuries, and hip fractures, making the subjects poor surgical candidates. The Talent Endovascular Graft was deployed via open femoral or iliac artery access under fluoroscopic guidance. All 4 patients underwent successful exclusion of their thoracic pseudoaneurysm with use of the Talent endovascular graft. One patient required partial coverage of the left subclavian artery, and a second patient had an iliac artery stent deployed after traversal of an area of stenosis with the delivery system. There were no cardiac, neurologic, pulmonary, or peripheral vascular complications. Acute aortic disruption, with its associated high surgical morbidity and mortality, is an excellent indication for endovascular therapy to improve patient outcomes. More long-term data are needed on repair durability. [ABSTRACT FROM AUTHOR]