Background-To further investigate vascular morphology and function in type 2 (non-insulin-dependent) diabetes mellitus (type 2D), small arteries were examined in vitro from carefully defined cohorts of patients with or without concomitant hypertension and the results compared with those from selected normotensive nondiabetic control subjects and a group of untreated patients with essential hypertension (EH). Methods and Results-Blood vessels were studied through the use of pressure myography to determine vascular morphology, mechanics, and myogenic responsiveness, together with testing of constrictor and dilator function. Small arteries from patients with EH demonstrated eutrophic inward remodeling and an increased distensibility. Vessels from type 2D patients demonstrated hypertrophy, a further increase in distensibility, and a highly significant loss of myogenic responsiveness compared with patients with EH and control patients. Vasoconstrictor function to norepinephrine was normal in patients with type 2D and type 2DϩH and EH. Endothelium-dependent dilation was normal in patients with EH but abnormal in patients with type 2D and type 2DϩH. There was a significant correlation between dilator impairment and the degree of dyslipidemia recorded in all groups. Conclusions-These results demonstrate vascular hypertrophy in small arteries from patients with type 2D. This could be a consequence of impaired myogenic responsiveness, which will increase wall stress for a given intraluminal pressure, which may be a stimulus for vascular hypertrophy. A substantial proportion of endothelial dysfunction can be attributed to an effect of the abnormal lipid profile seen in such patients. (Circulation. 2002;106:3037-3043.)

A contemporaneous multivariate prediction model for MACE after PCI was developed. The NWQIP tool allows calculation of the risk of MACE permitting meaningful risk adjusted comparisons of performance between hospitals and operators.

Abstract-Endothelial dysfunction has been demonstrated to occur in small arteries from patients with type 2 diabetes and hypertension. The effects of angiotensin II receptor blockade on vessel function were examined using pressure myography in a randomized 12-week double-blind placebo-controlled parallel group study using candesartan cilexitil. The maximal vascular response to acetylcholine (Ach) was impaired at baseline and improved with candesartan. This improvement was primarily caused by an effect in the nitric oxide component of Ach-mediated dilatation. The degree of endothelial dysfunction directly correlated with serum low-density lipoprotein cholesterol levels. Sodium nitroprusside-induced endothelium-independent dilatation was reduced in diabetic patients and intervention with candesartan lead to an improvement in EC50 with no change in maximal response.

A 63 year old man with a transvenous cardioverter-defibrillator, implanted in the rectus sheath, sustained a partial fracture of the right ventricular lead. We decided to replace the system with a pectoral "active can" device (Medtronic Jewel model 7219C) with a single tripolar ventricular lead. Attempts to remove the old right ventricular lead failed. We were unable to pass a guide wire to the superior vena cava and thought that the left subclavian . . . . . . vein was occluded. We resorted to a right subclavian vein approach, placing the lead in the body of the right ventricle ( figure).With a temporary "active can emulator" in the right pectoral region, the system terminated ventricular fibrillation, first at 24 J and then at 18 J. The defibrillation threshold one week later was satisfactory at <34 J with a defibrillation impedance of 55 Q.Recent reports have shown the efficacy of third generation transvenous implantable cardioverter defibrillators."2The system we used consists of a single tripolar right ventricular lead with the cover of the device acting as the anode. The manufacturers recommend that the device is implanted in the left pectoral region to facilitate the spread of the defibrillation wave across both the right and left ventricles. In our patient left sided implantation was precluded. However, defibrillation thresholds were satisfactory with the system implanted on the right side even though the vector between the cathode and anode predominantly passed through the right ventricle. The position of the right ventricular lead within the ventricle may be important. The figure shows that the new right ventricular lead is positioned away from the apex. This configuration may allow capture of more of the myocardium than an electrode placed at the right ventricular apex and so increase the probability of capturing enough myocardium3 to restore sinus rhythm.The feasibility of implantation of right sided "active can" system has not to the best of our knowledge been reported before.

drainage the patient's breathing improved and she was discharged home. However, she returned 3 weeks later with increasing shortness of breath. A repeat echocardiogram showed a small pericardial effusion (0.5 cm) and thoracic computed tomography (CT) revealed a dissecting aneurysm of the ascending aorta and aortic arch ( Figure 1). This was judged inoperable and she died 3 days later. J R Soc Med 1999;92:638-639 COMMENT As a complication of aortic dissection, haemorrhage into the pericardial sac with resultant cardiac tamponade is usually sudden and rapidly fatal1. We report a case in which the haemopericardium was chronic rather than acute. CASE HISTORYA previously fit and healthy woman aged 89 years gave a 5-week history of increasing shortness of breath and nonproductive cough without orthopnoea or paroxysmal nocturnal dyspnoea. 3 weeks ago she had had an episode of lower thoracic back pain, resolving over a few days, with poor appetite and some weight loss. On admission she was tachypnoeic with a temperature of 38.3°C. Pulse rate was 90/min, blood pressure 100/60mmHg with 15 mmHg paradox. All peripheral pulses were present and symmetrically equal; she had a pansystolic murmur radiating to the axilla, and on abdominal examination there was smooth 3 cm hepatomegaly. An