Patient reactions to cancelled or postponed heart operations.

Objectives The aim was to survey the rate and cause of cancellations of planned cardiac operations at a Swedish clinic during 1999, and to study how the patients were affected. Design Questionnaires were distributed to 74 patients who had their operations cancelled. Their mood after discharge was measured with The Hospital Anxiety and Depression scale. Ninety-three patients, who were operated on without postponement, served as controls. Results Sixty-one percent of the patients in the cancellation group reacted negatively, especially if the reason for cancellation was organizational (P = 0.03). The women in the cancellation group had a significantly higher degree of depression than men (P = 0.01) and both women (P = 0.02) and men (P = 0.003) in the control group. Most of the patients, however, were satisfied with the nursing staff's reception and information. Conclusions The patients reacted negatively to the cancellation, especially if it had organizational reasons. Women subjected to cancellation had a significantly higher degree of depression than other patients. To be avoided, organizational and medical problems must be identified in time. One way to do this is to introduce a preadmission nurse clinic

Increased expression of vascular endothelin type B and angiotensin type 1 receptors in patients with ischemic heart disease

<p>Abstract</p> <p>Background</p> <p>Endothelin-1 and angiotensin II are strong vasoconstrictors. Patients with ischemic heart disease have elevated plasma levels of endothelin-1 and angiotensin II and show increased vascular tone. The aim of the present study was to examine the endothelin and angiotensin II receptor expression in subcutaneous arteries from patients with different degrees of ischemic heart disease.</p> <p>Methods</p> <p>Subcutaneous arteries were obtained, by biopsy from the abdomen, from patients undergoing coronary artery bypass graft (CABG) surgery because of ischemic heart disease (n = 15), patients with angina pectoris without established myocardial infarction (n = 15) and matched cardiovascular healthy controls (n = 15). Endothelin type A (ET_A) and type B (ET_B), and angiotensin type 1 (AT₁) and type 2 (AT₂) receptors expression and function were examined using immunohistochemistry, Western blot and <it>in vitro </it>pharmacology.</p> <p>Results</p> <p>ET_Aand, to a lesser extent, ET_Breceptor staining was observed in the healthy vascular smooth muscle cells. The level of ET_Breceptor expression was higher in patients undergoing CABG surgery (250% ± 23%; P < 0.05) and in the patients with angina pectoris (199% ± 6%; P < 0.05), than in the healthy controls (100% ± 28%). The data was confirmed by Western blotting. Arteries from CABG patients showed increased vasoconstriction upon administration of the selective ET_Breceptor agonist sarafotoxin S6c, compared to healthy controls (P < 0.05). No such difference was found for the ET_Areceptors. AT₁and, to a lesser extent, AT₂receptor immunostaining was seen in the vascular smooth muscle cells. The level of AT₁receptor expression was higher in both the angina pectoris (128% ± 25%; P < 0.05) and in the CABG patients (203% ± 41%; P < 0.05), as compared to the healthy controls (100% ± 25%). The increased AT₁receptor expression was confirmed by Western blotting. Myograph experiment did however not show any change in vasoconstriction to angiotensin II in CABG patients compared to healthy controls (P = n.s).</p> <p>Conclusion</p> <p>The results demonstrate, for the first time, upregulation of ET_Band AT₁receptors in vascular smooth muscle cells in ischemic heart disease. These receptors may play a role in the pathophysiology of ischemic heart disease and could provide important targets for pharmaceutical interventions.</p

Eliminating the strong pulmonary vasoconstriction caused by Euro-Collins solution

Single-flush perfusion with Euro-Collins solution (ECS), after pretreatment with prostaglandin E1 or prostacyclin, is at most centers the standard procedure for preservation of lungs for transplantation. In a previous study, we showed that the high potassium content of ECS causes strong pulmonary vasoconstriction at temperatures higher than 20 degrees C. In the present study, five drugs used as pretreatment and added to the perfusate were compared for their ability to counteract ECS-induced constriction of porcine pulmonary arteries: papaverine reduced the vasoconstrictive effect by 92% +/- 4%; nifedipine, by 62% +/- 6%; the thromboxane A2 receptor antagonist daltroban, by 15% +/- 4%; and prostaglandin E1, by 12% +/- 4%. On the other hand, prostacyclin not only failed to reduce ECS-induced vasoconstriction but at the highest concentration tested, enhanced it by 37% +/- 7%. The combination of papaverine (10(-4) mol/L) and nifedipine (10(-6.5) mol/L) was the only pretreatment to abolish ECS-induced vasoconstriction; moreover, it has no adverse effect on endothelial function. Neither prostaglandin E1 nor prostacyclin effectively counteracts ECS-induced vasoconstriction, though they may have other beneficial effects

Pulmonary vascular resistance related to endothelial function after lung transplantation

In 8 donor pigs, flush perfusion was performed with a low-potassium-dextran solution. Ring segments were taken from a small intralobar pulmonary artery in the right lung immediately after perfusion and after 24 hours of cold storage for studies in organ baths. Stable vasoconstriction was induced with the thromboxane mimic U-46619, and acetylcholine was used to induce endothelium-dependent relaxation. The maximum relaxation was significantly reduced after flush perfusion compared with fresh nonperfused controls, and a significant additional reduction was seen after the 24-hour storage period. The left donor lung was transplanted into a recipient after 24 hours of cold storage. Contralateral pneumonectomy was then performed, making the recipient entirely dependent on the transplanted lung for survival. All 8 pigs were in good condition throughout the 24-hour observation period, with arterial oxygen tension of around 165 mm Hg (range, 80 to 275 mm Hg; inspired oxygen fraction, 0.5) and pulmonary vascular resistance of around 450 dyne.s.cm-5 (range, 260 to 730 dyne.s.cm-5). The maximum endothelium-dependent relaxation for each donor was checked for correlation to pulmonary vascular resistance and to systolic, mean, and diastolic pulmonary artery pressures as recorded at 4-hour intervals. Regression analyses showed arterial oxygen tension to be unrelated to pulmonary vascular resistance and endothelial dysfunction to be unrelated to pulmonary artery pressure but to correlate to pulmonary vascular resistance, this correlation being significant after reperfusion for 16 hours (p < 0.05) and highly significant after 24 hours (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS

Endothelium-dependent relaxation in pulmonary arteries after lung preservation and transplantation

Pulmonary hypertension is frequently seen after lung transplantation. To study how the release of the endothelium-dependent relaxing factor is affected by lung preservation and transplantation, porcine pulmonary arteries were investigated in organ baths. The arteries (1 mm in diameter) were taken from fresh nonperfused lungs (group I), lungs immediately after flush-perfusion with a low-potassium-dextran solution (group II), non-perfused lungs stored for 12 hours in low-potassium-dextran solution (group III), flush-perfused lungs stored for 12 hours in low-potassium-dextran solution (group IV), and group IV lungs after left lung transplantation and right pneumonectomy followed by 24 hours of reperfusion (group V). Stable contractions were induced with the thromboxane A2 analogue U-46619. Acetylcholine was used to stimulate the release of endothelium-dependent relaxing factor. In vessel segments where the endothelium had been removed, acetylcholine elicited no response. In segments with intact endothelium, acetylcholine induced concentration-dependent relaxation; the maximum relaxation obtained was 91% +/- 3% (I), 86% +/- 3% (II), 85% +/- 3% (III), 69% +/- 5% (IV), and 69% +/- 9% (V). Relaxation was significantly reduced in groups IV (p < 0.01) and V (p < 0.05) as compared with group I. Stable moderate pulmonary hypertension was present in all the transplanted lungs throughout the 24-hour observation period. It is concluded that the endothelium-mediated relaxation is significantly reduced after flush perfusion combined with 12 hours of storage in low-potassium-dextran solution. Lung transplantation, followed by 24 hours of reperfusion did not further impair the endothelium-dependent relaxation

Transapical versus transfemoral aortic valve implantation: a comparison of survival and safety.

Transcatheter aortic valve implantation (TAVI) is a therapeutic option for high-risk patients with aortic stenosis. Procedural mortality remains high in comparison with conventional aortic valve replacement (AVR) because patients determined for TAVI are commonly denied conventional surgery. We aimed to evaluate access-related complications between the transfemoral (TF) and the transapical (TA) approach and to compare survival between TAVI and conventional AVR in propensity-score-matched patients

Acute Kidney Injury Assessed by Cystatin C after Transcatheter Aortic Valve Implantation and Late Renal Dysfunction.

The aim of the present study was to evaluate acute kidney injury (AKI) with cystatin C following transcatheter aortic valve implantation (TAVI) and to assess the impact of postoperative AKI on outcome and late renal function

Might free arterial grafts fail due to spasm?

The rat femoral artery was used as a free graft and was studied after 2, 7, 14, 30, and 60 days. The patency of the grafts was 100% (2 days, n = 6), 78% (7 days, n = 9), 63% (14 days, n = 8), 33% (30 days, n = 12), and 18% (60 days, n = 11). Histology showed an intimal thickening after 14 days and the media, which in the controls consisted of eight to ten layers of myocytes, was reduced to six to eight cell layers. During the first 2 weeks the graft segments had an impaired contraction when exposed to Krebs solution with 124 mmol/L K+, whereas after 1 month and later the graft segments approached the controls or had even higher contractile force. The thromboxane mimic U-46619 elicited full contractile force at all times whereas the potency was significantly lower during the first 14 days. Noradrenaline was unable to induce contraction in the graft segments during the first 14 days, but at 30 and 60 days it had regained full contractile force and was significantly more potent (approximately 60 times) in the graft segments compared with the controls. This study suggests that intimal thickening and hypercontractility might be a problem in free muscular arterial grafts

Inhaled nitric oxide reveals and attenuates endothelial dysfunction after lung transplantation

BACKGROUND: Maintaining endothelial function within transplanted organs may be critical to successful preservation. In this study we have evaluated the relationship between the effect of inhalation of nitric oxide and the degree of endothelial dysfunction after lung transplantation. METHODS: A left lung, which had been preserved for 24 hours, was transplanted and a right pneumonectomy was performed in 5 pigs. After a 24-hour observation period the pigs inhaled 5, 20, and 80 ppm nitric oxide, and pulmonary vascular resistance was recorded continuously. From the same donors preserved pulmonary arteries from the contralateral lung were studied simultaneously in organ baths. Acetylcholine chloride was used to elicit endothelium-dependent relaxation in vessel segments contracted with the thromboxane A2 analogue U-46619. RESULTS: Maximal endothelium-dependent relaxation decreased in the preserved lungs and correlated to the pulmonary vascular resistance in the simultaneously transplanted lungs. Inhalation of nitric oxide in the pigs that had received transplants caused the pulmonary vessels to dilate in proportion to the endothelial dysfunction. CONCLUSIONS: Preservation of lung for transplantation induces an endothelial dysfunction, and the degree of the decrease in pulmonary vascular resistance caused by nitric oxide inhalation may be an indication of the degree of this endothelial damage. The vasodilation caused by inhaled nitric oxide increases as the endothelial function deteriorates