Vascular

The pathogenesis of the reperfusion syndrome is complex and as yet not fully elucidated. It is characterized by the development of increased microvascular permeability, oedema and tissue necrosis, and is associated with free radical release, cellular calcium overload and activation of neutrophils. Furthermore, systemic release of putative mediators may result in distant organ injury (lung, kidney, heart). This review, after briefly describing the role of neutrophils in these events, will concentrate on potential therapeutic interventions that might be employed to minimise ischaemia-reperfusion syndrome. Issues of safety will be considered, and potential applications of these techniques in patient management discussed.

Monocyte infiltration into forming thrombus has been demonstrated in experimental models of venous thrombosis developed in our laboratories. These cells produce and release plasminogen activators as the thrombus organises and resolves. Monocytes are also capable of assembling and releasing procoagulant factors and the evidence for their importance in thrombogenesis is reviewed. The ability of monocytes to maintain this fibrinolytic balance suggests that they may have a role in both thrombosis and thrombus resolution. Control of the mechanisms which regulate these activities may therefore be important in preventing thrombus formation or stimulating its resolution.

Several studies have shown that mitral valve replacement with total chordal preservation (MVR-TCP) improves left ventricular function when compared with total chordal transection. Few clinical studies, however, have compared this technique to that involving only posterior chordal preservation (MVR-PCP). This study was intended to cover this aspect. A total of 36 consecutive patients with chronic rheumatic mitral incompetence were operated upon by one surgeon and benefited from MVR-TCP (group I). During the same period and along similar selection criteria, 60 patients underwent MVR-PCP (group II) in our department. With the exception of a statistically significant higher preoperative left ventricular ejection fraction (LVEF) percentage and lower fractional shortening (LVFS) percentage in group II patients; both groups were comparable as regarding age, sex distribution New York Heart Association (NYHA) functional class (FC). preoperative left atrial diameter (LAD), left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic dimension (LVESD) as well as aortic cross-clamp and cardiopulmonary bypass times. The means of the differences, between the pre- and postoperative values of NYHA FC and echocardiographic data were compared between both groups. As compared with group II, group I patients showed lower: hospital mortality rate (0 versus 8.3%; P > 0.05); need for positive inotropic support (11.1 versus 20.8%; P > 0.05) and total ICU stay (2.9 ± 0.17 versus 2.2 ± 0.13 days; P < 0.01). In addition, group 1 patients showed a better NYHA FC improvement (−2.08 ± 0.15 versus −1.93 ± 0.11; P > 0.05) as well as a statistically significant (P < 0.00001) higher decrease in the LAD (−18.19 ± 0.97 versus −11.59 ± 0.58 mm). LVEDD (−14.44 ± 0.91 versus −6.17 ± 0.05 mm). LVESD (−6.17 ± 0.77 versus −3.23 ± 0.01 mm), LVFS percentage (−0.06 ± 0.01 versus −0.01 ± 0.001%) and a higher increase in the LVEF percentage (8.1 ± 0.9 versus 1.48 ± 0.02%). The smaller mean diameter of the implanted St Jude prosthesis, in group I patients (26.77 ± 0.22 versus 27.43 ± 0.21 mm; P = 0.046), was neither associated with the use of a smaller prosthesis than that predicted for the patient size nor a significantly higher mean transprosthetic pressure gradient. These data suggest that in rheumatic patients with chronic mitral incompetence, MVR-TCP is always feasible: it is associated with lower hospital mortality and morbidity rates and better preservation of the postoperative left ventricular systolic functions when compared with MVR-PCP.

In the years 1994 and 1995, 1087 patients underwent coronary artery bypass grafting at our institution. Of these, 297 were operated on without cardiopulmonary bypass. 239 were male, and 58 were female. Their ages ranged from 28 to 81 years (54.43 ± 9.63). Of the total, 294 were operated on electively, two as a coronary reoperations, and one as an emergency after a failed percutaneous transluminal coronary angioplasty procedure. In all patients complete revascularization was the aim, and a cardiopulmonary bypass team was kept on standby. Median sternotomy was performed as the exposure in all patients, except a patient who underwent a coronary reoperation through a left thoracotomy incision. The average of the distal anastomoses was 1.51 ± 0.6, ranging from 1 to 3. The left internal thoracic artery was used in 292 operations, which was an individual graft in 284, a sequential graft in five, and a free graft in four. Major complications in the early postoperative period were noted in three patients as reoperation for excessive bleeding. One patient had reoperation for left internal thoracic artery spasm, and one patient had lower extremity ischemia caused by intraoartic balloon counterpulsation. Hospital mortality was 0.3% with one patient. It is our belief that in selected cases coronary artery bypass grafting without cardiopulmonary bypass is a safe procedure with the advantage of improvement in recovery during the postoperative period.

L-Carnitine has been shown to improve the post-ischemic recovery of myocardial function and metabolic measurements that are reduced in the course of ischemia and reperfusion of the heart. In this study we used 40 male guinea-pigs in order to determine if the effect of L-carnitine which is used in the protection of the post-ischemic reperfused heart, is dose-dependent or not. All harvested hearts were perfused for 30 min on modified Langendorf apparatus with oxygenized Krebs–Henseleit solution. After this period, in (n = 10), 5 mmol and 10 mmol (group B, n = 10) of L-carnitine were added into a Krebs–Henseleit solution. After 20 min, perfusion was complete and the hearts were then exposed to normothermic ischemia for 20 minutes. Following the ischemia, hearts were reperfused with the same solutions for 30 min. In group C (n = 10), 10 mmol of L-carnitine was added into the solution at the post-ischemic reperfusion step. In the control group, the same procedures were performed without using L-carnitine. Matching was done according to the contractile force of the heart rate and the levels of malondialdehyde and adenosine deaminase. When 10 mmol L-carnitine was added into the perfusion solutions at the pre-ischemic period, the best results were obtained and myocardial damage was much less than the control group. The protective effects of L-carnitine in normothermic ischemia is dose-dependent and it must be given at the pre-ischemic period.

In order to predict tissue viability in infarcted myocardial areas, changes induced by nitroglycerine infusion on Sestamibi myocardial uptake were evaluated in 37 patients with previously confirmed myocardial infarction undergoing coronary artery bypass grafting, and compared with echocardiographic and perfusional changes occurring after the operation. The improvement of Sestamibi uptake after nitroglycerine correctly classified 24/26 (92%) patients showing postoperative improvement of wall motion in the infarcted area, whereas 24/31 (77%) patients with nitroglycerine-induced increase in Sestamibi uptake had improved wall motion after operation. The presence of collateral flow to the infarcted area was associated with a significantly (P < 0.01) higher increase in Sestamibi uptake both during nitroglycerine infusion and postoperatively. An increase in wall motion score after operation was associated with a significantly higher (P < 0.05) increase in Sestamibi uptake score during nitroglycerine infusion. Thus, the results of this study suggest that Sestamibi perfusional myocardial scintigraphy during nitroglycerine infusion is capable of assessing viable but chronically hypoperfused myocardium and predicting postoperative wall motion and perfusional improvement, to yield the best results in patients with evidence of collateral circulation that supplies the infarcted area.

Optimal surgical strategy in patients with concomitant coronary and carotid artery disease is debatable. We have analysed 15-years of experience (January 1981-August 1996) with 195 consecutive patients in whom we have used two different surgical approaches. Group A consisted of 48 patients who underwent a single-stage surgical procedure, and group B (147 patents) underwent a two-stage procedure, either as carotid endarterectomy followed by coronary artery bypass surgery (group B₁, 97 patients), or as coronary artery bypass surgery followed by carotid endarterectomy (group B₂, 50 patients). Overall, there were 40 (20.5%) patients with left main coronary artery disease, 49 (25.1%) with poor left ventricular function, 128 (65.6%) with previous myocardial infarction, 134 (68.7%) were in New York Health Authority (NYHA) functional class III or IV, and bilateral carotid involvement was present in 57 patients (29.2%). Unstable angina was more frequent in groups A and B₂ (P < 0.0001), NYHA class III-IV was more frequent in group A (versus B₁, P = 0.001 and versus B₂, P = 0.02), low ejection fraction (EF) was more frequent in groups A and B₂ (P < 0.0001 for both), bilateral carotid stenosis in groups A and B₁ (P = 0.02 and P = 0.0001, respectively) and ulcerated plaque in group B₁ (versus A, P = 0.0001). These differences dictated the surgical strategy, which resulted in different protocols for clinical and operative management.

From 1990 to 1995, 12 patients with cavo-atrial renal cell carcinoma underwent resection of the tumor. Circulatory arrest was employed in 11/12 cases. The neoplasm extended to the inferior vena cava in two patients and to the intrahepatic veins or right atrium in five cases. Two severely cardiac compromised patients died perioperatively. Of five patients who showed preoperative suspicion of isolated metastases, 3 patients died postoperatively because of relapsing disease after a mean period of 10.8 months. Five patients are alive and doing well after a mean follow-up of 14.8 months. In our experience myocardial dysfunction determined poor immediate survival. Mid-term survival was influenced by preoperative metastases and lymph-node involvement, but not by intracaval extension. Circulatory arrest appears to be a relatively safe technique to remove renal carcinoma with cavo-atrial extension and should be indicated whenever there are no metastases.

The aim of this study was to determine any biochemical differences between early-onset peripheral vascular disease and typical onset atherosclerosis, and age-matched controls. A subset of patients present at a young age (< 50 years) with peripheral vascular disease which pursues an aggressive course. As lipid oxidation seems important in atherosclerosis, total lipid peroxides, oxidized subfractions, and Trolox equivalent antioxidant capacity (TEAC) were studied in patients with premature peripheral vascular disease. Charts were reviewed of patients operated on for vascular occlusive disease over a 5-year period. Patients with early-onset peripheral vascular disease (group I) were evaluated for biochemical abnormalities and compared with typical onset atherosclerotics (group II) and age-matched controls (group III). Sixteen patients with early-onset peripheral vascular disease underwent biochemical evaluation. Conventional lipid profiles did not differ statistically from those of age-matched controls, except for mild elevations in LDL and VLDL in patients with vascular occlusive disease (207 and 195 mg/dl in groups I and II versus 157 mg/dl in group III). Total oxidative potential was significantly elevated (P = 0.006) 3.04, 2.15 and 2.04 nmol/ml in groups I, II and III, respectively. Levels of oxidized LDL and VLDL were even more significantly elevated (P = 0.0009) for premature peripheral vascular disease, (1.2, 0.58 and 0.47 nmol/ml in groups I-III). TEAC values did not differ significantly between groups (0.83, 0.82, 0.82 nmol/ml) and did not correlate with total lipid peroxide values for individual patients. In conclusion, lipid peroxides were significantly elevated in patients with premature peripheral vascular disease, the most marked changes being seen in oxidized LDL and VLDL subfractions. Lipid peroxides were elevated when standard lipid profiles were only mildly abnormal. The poor long-term prognosis in these patients suggests the need for aggressive evaluation and treatment of lipid abnormalities.

The incidence and indications for conversion from endoluminal to open repair of abdominal aortic aneurysms are changing. This paper is based on a 5-year experience in which endoluminal repair of abdominal aortic aneurysms was undertaken in 156 patients. Primary conversion at the original operation was required in 14 patients and secondary conversion at a subsequent operation was required in 9 patients. The reasons for primary conversion were access problems (n = 2), balloon related problems (n = 2), endograft migration (n = 4), endograft thrombosis (n = 1) and failed deployment of a bifurcated endograft (n = 5). Twelve of 14 primary conversions occurred in the first half of the study period, in which 59 endoluminal abdominal aortic aneurysms repairs were undertaken. Improvements in technology and interventional techniques for overcoming obstacles, as well as increasing experience, has resulted in primary conversion being limited to two patients in the most recent 2.5-year period in which 97 endoluminal repairs were undertaken. The reasons for secondary conversion were renal arteries covered by the endograft (n = 2), increasing abdominal aortic aneurysm diameter in the absence of endoleak (n = 1) and persistent endoleak (n = 6). The latter group comprised three patients with intact aneurysms and three with known endoleaks who presented with ruptured aneurysms. The current indications for primary conversion include: (i) rupture of the aorta; (ii) complete migration of the endograft resulting in obstruction of the iliac arteries; and (iii) irreversible twisting of a non-modular bifurcated endograft. The current indications for secondary conversion include: (i) persistent endoleak; (ii) sealed endoleak with continued abdominal aortic aneurysms expansion; (iii) apparently successful endoluminal repair without evidence of endoleak but continued abdominal aortic aneurysms expansion; and (iv) infected endograft.