ST-Segment Elevation Myocardial Infarction and Right Atrial Myxoma.

Background Cardiac myxoma is the most common primary cardiac tumor. Although benign, it can cause life-threatening complications due to embolization. Case Presentation We describe an ST-elevation myocardial infarction (STEMI) involving a giant right atrial myxoma and persisting foramen ovale (PFO) in a 64-year-old male patient and report on emergency percutaneous interventional therapy and subsequent cardiac surgery to remove the right atrial myxoma. Conclusion A right atrial myxoma, combined with a PFO, can cause a STEMI. Therefore, every acute coronary syndrome patient should undergo ultrafast exploratory emergency echocardiography to protect the physician from unpleasant surprises.

Giant Intramural Right Ventricular Hematoma after PCI in a Patient with Condition after CABG.

Coronary artery perforation secondary to percutaneous coronary intervention (PCI) is a rare, but a potentially life-threatening complication. There is a misconception that cardiac tamponade rarely occurs in patients with prior coronary artery bypass grafting (CABG). We first describe a giant right ventricular intramural hematoma following PCI via a saphenous vein graft to treat a distal stenosis of the right coronary artery, and its successful treatment with redo cardiac surgery. Complex elective PCIs on patients after CABG should be performed in specialized centers with a well-established heart team that has the expertise to treat any of the potential complications.

L-arginine protects the mesenteric vascular circulation against cardiopulmonary bypass-induced vascular dysfunction.

BACKGROUND: The aim of our study was to determine whether addition of the nitric oxide donor l-arginine at reperfusion may prevent the cardiopulmonary bypass (CPB)-induced vascular alterations in the intestine. METHODS: Twelve dogs underwent 90-minute hypothermic CPB. After 60 minutes, the cardiac arrest-treated group (n = 6) received 40 mg/kg intravenous bolus l-arginine, followed by 3 mg/kg/min infusion for 20 minutes. Hemodynamic parameters, blood gases, lactate, and glucose were monitored. Reactive hyperemia (RH) in response to superior mesenteric artery ischemia and vasorelaxation to systemically administered vasoactive drugs (acetylcholine [ACH] and sodium nitroprusside) were assessed before and after CPB and defined as percent change of vascular resistance. RESULTS: In the control group, CPB reduced reactive hyperemia (RH) (-26 +/- 15% vs -53 +/- 5%), and the response to ACH (-30 +/- 3% vs -42 +/- 7%). In the treated group, the post-CPB endothelial dysfunction was reversed (-37 +/- 1%, P <.05 vs control group) and RH partially recovered (-34 +/- 4%, P <.05). Administration of l-arginine resulted in a higher mesenteric oxygen delivery, increased nitrite/nitrate production, and lower lactate release from the mesenteric vascular circulation after reperfusion. CONCLUSIONS: CPB disrupts some of the regulatory functions of the endothelial cell in the mesenterium and these are mostly related to nitric oxide unavailability. Systemic supplementation of l-arginine at reperfusion prevents the CPB-induced mesenteric endothelial dysfunction in association with an increased blood distribution and a reduced metabolic impairment.

Mesenteric complications after hypothermic cardiopulmonary bypass with cardiac arrest: underlying mechanisms.

The aim of this study was to determine the pathophysiological mechanisms of postcardiopulmonary bypass (CPB) intestinal dysfunction using an in vivo canine model of extracorporeal circulation. Six dogs underwent a 90 min hypothermic CPB with continuous monitoring of mean arterial blood pressure (MAP) and mesenteric blood flow (MBF). Reactive hyperemia and vasodilator responses of the superior mesenteric artery to acetylcholine and sodium nitroprusside were determined before and after CPB. Mesenteric lactate production, glucose consumption, creatine kinase (CK) release and venous free radicals were determined. CPB induced a significant fall (p < 0.05) in MAP and MBF. After CPB, reactive hyperemia (-26 +/- 15% versus -53 +/- 2%, p < 0.05) and the response to acetylcholine (-42 +/- 9 versus -55 +/- 6%, p < 0.05) were significantly decreased. Reperfusion increased lactate production (0.8 +/- 0.09 mmol/L versus 0.4 +/- 0.18, p < 0.05) and the CK release (446 +/- 98 U/L versus 5 +/- 19 U/L, p < 0.01). Endothelial dysfunction, conversion from aerobic to anaerobic metabolism, and intestinal cell necrosis seem to be responsible for intestinal complications associated with CPB.