Nicorandil-induced peripheral vasodilatation during cardiopulmonary bypass.

Nicorandil is an antianginal agent with actions at epicardial coronary arteries and arterioles, systemic arterioles, and veins. We report our experience with 7 patients taking oral Nicorandil who had severe vasodilation and hypotension requiring significant vasoconstrictor support after cardiopulmonary bypass. Although the mechanism for this phenomenon remains unknown Nicorandil might be interacting with other factors present during cardiopulmonary bypass, as it has relatively mild hemodynamic effects outside this situation.

Dichotomy in the post-ischemic metabolic and functional recovery profiles of isolated blood-versus buffer-perfused heart.

There is evidence that buffer- and blood-perfused hearts differ in their postischemic functional recoveries. The present study was designed to: (i) compare ischemia-induced contracture and post-ischemic functional recovery, and (ii) investigate whether the recovery profiles were related to either the release of purines and norepinephrine or high-energy phosphate content. Rat hearts (n = 8/group) were perfused at 37 degrees C with buffer (60 mmHg) or blood (60 mmHg from a support rat), made globally ischemic (15 min) and reperfused (15 min). The onset and severity of ischemic contracture were identical in both models [left ventricular end-diastolic pressure (LVEDP) at the end of 15 min ischemia was 30 +/- 5 and 27 +/- 4 mmHg respectively; P = N.S.]. However, the rate and extent of post-ischemic left ventricular developed pressure (LVDP) differed considerably. Blood-perfused hearts exhibited an initial rapid and complete recovery of LVDP followed by a steady decline to approximately 60% of pre-ischemic values. Buffer-perfused hearts recovered to only 80% after 5 min reperfusion and remained at this level for the duration of reperfusion LVEDP was higher in buffer-perfused than in blood-perfused hearts during the first 5 min of reperfusion; thereafter, LVEDP fell in buffer-perfused hearts to a level than was not significantly different from the observed in blood-perfused hearts. In buffer-perfused hearts, coronary flow recovered to 90% within 5 min and then remained constant; in blood-perfused hearts flow recovered to 100% by 1 min and continued to rise to a maximum by 7 min (201 +/- 15%). This increase appeared to mirror the secondary decline in LVDP. During the first 4 min of reperfusion, in both preparations, venous norepinephrine increased to six- to nine-fold of pre-ischemic values and then fell rapidly to near control levels by 6-9 min. Total purine release was high in early reperfusion in both groups. At the end of 15 min reperfusion, the tissue adenylate pool was similar in both groups. This study demonstrates that the nature of the perfusate used for an isolated rat heart preparation: (i) does not appear to influence the severity of ischemic injury as assessed by ischemic contracture, but (ii) does influence the qualitative and quantitative characteristics of the temporal profile that describes the recovery of systolic and diastolic function during the first 15 min of reperfusion: and (iii) it has no effect upon the changes seen in a number of metabolic indices that are often used for the assessment of injury and protection.

Effects of cardioplegia on vascular function and the "no-reflow" phenomenon after ischemia and reperfusion: studies in the isolated blood-perfused rat heart.

The ability of cardioplegia to protect against cardiac contractile dysfunction caused by ischemia and reperfusion is well established. The effects of cardioplegia on vascular injury and the no-reflow phenomenon, however, remain controversial. We used the blood-perfused rat heart to study the effect of St. Thomas' Hospital cardioplegic solution on postischemic endothelium-dependent and endothelium-independent vascular function, the extent of the no-reflow phenomenon, and the temporal relationship between postischemic vascular and contractile function. Isolated rat hearts (16 per group) perfused with blood from a support rat at 60 mm Hg were subjected to 10, 20, 30 or 40 minutes of global ischemia and 40 minutes of reperfusion at 37 degrees C. Eight hearts in each group also received cardioplegia (45 mm Hg for 2 minutes) before ischemia. Left ventricular developed pressure was measured with an intraventricular balloon. At the end of reperfusion, a bolus of 250 micrograms nitro-L-arginine methyl ester was infused to assess endothelium dependent vascular function. After a 20-minute washout, 25 micrograms sodium nitroprusside was infused to assess endothelium-independent vascular function. Fluorescein (1 ml, 1% weight/volume) was then infused to assess no-reflow; this involved freezing the hearts, cutting them into transverse sections (10 x 1 mm), video recording the sections under ultraviolet light, digitizing the images, and analyzing density of fluorescence. No-reflow was defined as a flow of less than 5%. Compared with nonischemic control responses, endothelium-independent vascular function was significantly decreased only after 30 and 40 minutes of ischemia (48.1% +/- 3.8% and 24.3% +/- 7.4%, p < 0.05), but it was significantly protected by cardioplegia (66.6% +/- 3.9% and 64.5% +/- 5.2%, p < 0.05). A significant reduction in endothelium-dependent vascular function was observed after 40 minutes of ischemia (-31.8% +/- 6.6% vs -50.4% +/- 1.6% in control hearts, p < 0.05), and again this was improved by cardioplegia (-45.0% +/- 3.4%, p < 0.05 vs ischemic group). Areas of no reflow were present after 30 and 40 minutes of ischemia (11.9% +/- 6.8% and 33.4% +/- 14.1% of left ventricular mass), and at each time period they were significantly decreased by cardioplegia (0.7% +/- 0.4% and 3.8% +/- 1.6%, p < 0.05). Postischemic contractile dysfunction was observed before any vascular alteration was apparent. After only 20 minutes of ischemia, the postischemic recovery of left ventricular developed pressure fell to 56.7% +/- 4.0%, but both endothelium-dependent vascular function and endothelium-independent vascular function were unaffected. In conclusion, vascular alterations are apparent only after prolonged periods of ischemia, longer than those required to observe contractile dysfunction, and cardioplegia protects against postischemic endothelium-dependent and endothelium-independent vascular dysfunction and reduces the extent of the no-reflow phenomenon.

Can ischemic preconditioning ensure optimal myocardial protection when delivery of cardioplegia is impaired?

BACKGROUND: Ischemic preconditioning is a potent protective intervention that is effective in all species studied. We have previously shown it to be as effective as cardioplegia; however, we have also shown that their combined use does not afford greater protection than the use of either alone. In the present study we investigated whether coincident ischemic preconditioning could compensate for inadequate cardioplegic protection when the delivery of cardioplegia was impaired, such as occurs in the presence of severe coronary stenosis or occlusion. METHODS AND RESULTS: Isolated rat hearts were subjected to 30 minutes of global ischemia followed by 40 minutes of reperfusion. Four groups of hearts (n = 12 per group) were studied: group 1, controls (no intervention); group 2, cardioplegia administered to hearts with a proximally occluded coronary artery; group 3, ischemic preconditioning applied before ischemia; and group 4, ischemic preconditioning and cardioplegia given in combination to hearts with a proximally occluded coronary artery. The postischemic recovery of left ventricular (LV) developed pressure (LVDP), expressed as a percentage of preischemic values, was significantly greater (P < .05) in preconditioned hearts (64 +/- 3%) than in control hearts (24 +/- 4%) or hearts treated with suboptimal cardioplegia (43 +/- 5%). Hearts with preconditioning plus cardioplegia recovered to an extent similar to that seen with preconditioning alone (59 +/- 2%). LV end-diastolic pressure was greater in control hearts (58 +/- 4 mm Hg) than in hearts with cardioplegia (41 +/- 4 mm Hg; P < .05 versus group 1) despite the incomplete delivery of the cardioplegia; the best protection was observed in preconditioned hearts and hearts with preconditioning plus cardioplegia (24 +/- 1 and 26 +/- 2 mm Hg, respectively; P < .05 versus groups 1 and 2). CONCLUSIONS: When the delivery of cardioplegia was impaired, myocardial protection (postischemic LVDP) was better served by ischemic preconditioning. Under the same conditions, the combination of cardioplegia plus preconditioning afforded superior protection compared with cardioplegia alone. These results may be of clinical interest since most patients who undergo surgery for ischemic heart disease suffer from severe coronary artery lesions that can prevent the adequate delivery of cardioplegia.

Cor triatriatum sinister, not mitral stenosis, in an adult with previous Sydenham's chorea: diagnosis and preoperative assessment by cross sectional echocardiography.

In cor triatriatum sinister, one of the rarest congenital cardiac anomalies, a membrane divides the left atrium into a pulmonary venous component above and the vestibule below. The importance of the anomaly lies in the effects of the resultant pulmonary venous obstruction that usually present in the first year of life and can mimic obstructed total anomalous venous drainage or congenital mitral stenosis. A case presented as mitral stenosis in the third decade of life, ten years after a well documented episode of Sydenham's chorea. The diagnosis was made rapidly by transthoracic echocardiography and transoesophageal echocardiography was used for complete assessment. Cardiac catheterisation added nothing to the non-invasive diagnosis or the preoperative assessment. Uncomplicated corrective surgery was undertaken.

Oesophageal erosion of an Angelchik prosthesis: surgical management using fundoplication.

Complications following insertion of the Angelchik prosthesis are becoming increasingly recognised. We report a 35-year-old patient with both mediastinal migration and intraluminal oesophageal erosion of a prosthesis. Successful management included transthoracic removal combined with a modified onlay fundoplication over the oesophageal defect to prevent gastro-oesophageal reflux.