Fabrizio Tomai

Ischemic preconditioning during coronary angioplasty is prevented by glibenclamide, a selective ATP-sensitive K+ channel blocker.

BackgroundBrief episodes of ischemia render the heart more resistant to subsequent ischemia; this phenomenon has been called ischemic preconditioning. In some animal species, myocardial preconditioning appears to be due to activation of ATP-sensitive K+ (KATP) channels. The role played by KATP channels in preconditioning in humans remains unknown. The aim of this study was to establish whether glibenclamide, a selective KATP channel blocker, abolishes the ischemic preconditioning observed in humans during coronary angioplasty following repeated balloon inflations. Methods and ResultsTwenty consecutive patients undergoing one-vessel coronary angioplasty were randomized to receive 10 mg oral glibenclamide or placebo. Sixty minutes after glibenclamide or placebo administration, patients were given an infusion of 10% dextrose (8 mL/min) to correct glucose plasma levels or, respectively, an infusion of saline at the same infusion rate. Thirty minutes after the beginning of the infusion, both patient groups underwent coronary angioplasty. The mean values (± 1 SD) of ST-segment shifts on the surface 12-lead ECG and the intracoronary ECG were measured at the end of the first and second balloon inflations, both 2 minutes long. In glibenclamide-treated patients, the mean ST-segment shift during the second balloon inflation was similar to that observed during the first inflation (23± 13 versus 20±8 mm, P=NS), and the severity of cardiac pain was greater (55±21 versus 43±23 mm on a scale of 0 to 100, P<.05). Conversely, in placebo-treated patients the mean ST-segment shift during the second inflation was less than that during the first inflation (9±5 versus 23±13 mm, P<.001), as was the severity of cardiac pain (15±15 versus 42±19 mm, P<.01). Blood glucose levels were significantly reduced 60 minutes after glibenclamide compared with those at baseline (53±9 versus 102±10 mg/100 mL, P<.001) in the glibenclamide group; however, before coronary angioplasty, blood glucose levels increased to 95±19 mg/100 mL, a value similar to that found in placebo group (96±11 mg/100 mL, P=NS). ConclusionsIn humans, ischemic preconditioning during brief repeated coronary occlusions is completely abolished by pretreatment with glibenclamide, thus suggesting that it is mainly mediated by KATP channels.

Left ventricular decompression through a patent foramen ovale in a patient with hypertrophic cardiomyopathy: a case report

The foramen ovale is considered an unidirectional flap-like valvular structure. Yet, it may increase in size and allow a continuous left-to-right shunt in order to reduce left ventricular filling pressures.We report the case of a 63-year-old woman with hypertrophic cardiomyopathy, referred for percutaneous closure of a coexisting secundum atrial septal defect. Before catheterization, however, transesophageal echocardiography revealed a continuous left-to-right shunt within the atrial septum, thus suggesting the diagnosis of patent foramen ovale with stable left-to-right shunt. At catheterization, performed under general anesthesia and transesophageal echocardiographic monitoring, left ventricular early- and end-diastolic pressures were 2 and 12 mmHg and pulmonary-to-systemic flow ratio was 1.4. Provocative maneuvers were not able to reverse the shunt. In order to assess the effect of the increased left ventricular preload due to the abolition of the shunt, an Amplatzer sizing balloon was inflated for 5 minutes across the patent foramen ovale. Diastolic pressures rose up to 5 and 18 mmHg, respectively. Such a worsening of left ventricular function suggested us not to perform the closure procedure.Transcatheter closure of any interatrial communication with stable left-to-right shunt induces an abrupt overload of the left ventricle that may cause acute heart failure in patients with coexisting left ventricular dysfunction. The hemodynamic evaluation of left ventricular function during transient abolition of the shunt is an useful tool in order to establish the most correct therapeutic strategy. The closure procedure should not be performed if a worsening of left ventricular function occurs.

Coronary flow reserve early and late after minimally invasive coronary artery bypass grafting in patients with totally occluded left anterior descending coronary artery

BACKGROUNDnThe impairment of flow reserve of the left anterior descending coronary artery in the early postoperative period in patients receiving a left internal thoracic artery graft has been related to the effects of cardiopulmonary bypass. Indeed, the late improvement in flow has been attributed to a late increase in left internal thoracic artery diameter.nnnMETHODSnWe evaluated 12 patients who underwent minimally invasive direct coronary artery bypass surgery with the internal thoracic artery used to graft an occluded left anterior descending artery without extracorporeal circulation. Early and 6 months after the operation, patients underwent a second angiogram of the left internal thoracic artery graft and assessment of coronary flow reserve by use of an intracoronary 0.014-inch Doppler guide wire.nnnRESULTSnAt the late study, coronary flow reserve had increased compared with the early postoperative data from 1.8 +/- 0.4 (standard deviation) to 2.5 +/- 0.6 (P =.002) because of a significant decrease in baseline averaged peak velocity (32.4 +/- 6.2 vs 21.3 +/- 6.4 cm/s, P =.002), whereas the hyperemic values were similar (51 +/- 6 vs 53.7 +/- 21.9 cm/s, P =.6). The diameters of the thoracic artery (2.1 +/- 0.3 vs 2.2 +/- 0.3 mm, P =. 7) and the left anterior descending coronary artery (1.8 +/- 0.1 vs 1.8 +/- 0.2 mm, P =.5), as well as myocardial oxygen consumption (106 +/- 14 vs 101 +/- 16 mm Hg. beats/min. 10(-2), P =.5), were unchanged.nnnCONCLUSIONSnOur findings suggest that the late improvement in coronary flow reserve is independent of the diameter of the graft and probably reflects an early distal coronary vessel dysfunction, which normalizes with time.

Early coronary artery bypass graft thrombosis in a patient with protein S deficiency

A 59-year-old white man underwent multiple coronary artery bypass grafts (CABGs) on an emergency basis for severe stenosis of the left main, and occlusion of the right coronary, artery. One month after operation recurrence of angina prompted a new diagnostic evaluation. Occlusion of the grafts was detected at angiography. Accurate hematological screening before reoperation showed decreased levels of protein S. One year after his second operation, the patient is asymptomatic on oral anticoagulant therapy. Tallium-201 scintigraphy shows normal myocardial perfusion.

Postoperative transient internal thoracic artery pseudoaneurysm.

Early after beating-heart coronary artery surgery several anecdotal patients are reported to have significant irregularities at the site of coronary anastomoses. These irregularities are shown at early postoperative angiography as filling defects of contrast medium inside the coronary vessel. These filling defects, most probably caused by small thrombi, have been related to improper intraoperative anticoagulation or to snaring the coronary vessel during the surgical procedure. Such defects are transient and, after spontaneous thrombolysis, are not evident on later angiograms. We present a case of left internal thoracic artery graft pseudoaneurysm found at angiography the day after a beating-heart coronary artery surgery procedure (Fig 1). After 1 month, repeat angiography revealed complete thrombosis of the pseudoaneurysm and a normally functioning coronary anastomosis (Fig 2). As for filling defects, in patients with small pseudoaneurysms it seems wiser to withhold further interventional procedures (stenting, surgical clipping) for at least 1 month before repeating coronary angiography. Address reprint requests to Dr De Paulis, Cattedra di Cardiochirurgia, Universita di Roma “Tor Vergata,” European Hospital, via Portuense 700, 00149 Roma, Italy; e-mail: depauli@tin.it. Fig 1. Fig. 2.