Predictive value of C-reactive protein in patients with unstable angina pectoris undergoing coronary artery stent implantation

This study was aimed at establishing the relation between baseline C-reactive protein levels and 12-month outcome in patients with unstable angina successfully treated with coronary artery stent implantation. Our results suggest that in patients with unstable angina and 1-vessel coronary disease successfully treated with coronary artery stent implantation, normal baseline serum levels of C-reactive protein identify a subgroup of patients at low risk of cardiac events during follow-up.     

Iliac arteriovenous fistula complicating lumbar laminectomy

An iliac arteriovenous fistula may rarely complicate lumbar laminectomy, particularly at the L4-L5 level. We present such a complication in a 45-year-old man who presented in our institution with a postlaminectomy iliac arteriovenous fistula and severe congestive heart failure. Repair of the fistulous orifice and tubular reconstruction of the iliac artery were successfully performed.     

Diastolic time during exercise in normal subjects and in patients with coronary artery disease. A plethysmographic study

Percent diastole (%D) was evaluated at rest and during effort (submaximal upright exercise) in 13 normal subjects and in 14 age-matched patients with coronary artery disease (CAD). Systolic time intervals were also simultaneously recorded by using the thermistor pulse transducer. At rest, in both groups, a positive linear regression was found between %D and cycle length (RR) (%D = 19.1 + 0.044RR, r = 0.83 in normals; %D = 21.2 + 0.044RR, r = 0.88 in CAD). During effort, while in normals no correlation was found between %D and RR values, in CAD patients %D and RR were linearly related (%D = -12.81 + 0.087RR, r = 0.67). These results prove that diastolic time is differently affected by the exercise in the two examined groups and that in CAD patients an abnormal reduction of %D occurs during stress test.     

Effects of hydroxymethylglutaryl coenzyme A reductase inhibitor simvastatin on smooth muscle cell proliferation in vitro and neointimal formation in vivo after vascular injury

OBJECTIVES: We sought to evaluate the effects of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors on vascular smooth muscle cell (VSMC) proliferation in vitro and neointimal formation in vivo after vascular injury. BACKGROUND: Neointimal hyperplasia after vascular injury is responsible for restenosis after arterial stenting, whereas arterial remodeling and neointimal formation are the causes of restenosis after percutaneous transluminal coronary angioplasty. METHODS: We assessed the effect of simvastatin on in vitro VSMC proliferation. To study the effects of simvastatin in vivo, balloon injury and stent deployment were performed in the common carotid artery of rats. Neointimal area was measured two weeks later in the balloon injury model and three weeks after stent deployment. RESULTS: Simvastatin markedly inhibits VSMC proliferation in vitro. In vivo, simvastatin reduced, in a dose-dependent manner, the neointimal area and the neointima-media ratio after balloon injury from 0.266 +/- 0.015 mm2 to 0.080 +/- 0.026 mm2 and from 1.271 +/- 0.074 to 0.436 +/- 0.158 (p < 0.001 vs. control rats) at the highest dose. Simvastatin also significantly reduced the neointimal formation and the neointima-media ratio after stenting from 0.508 +/- 0.035 mm2 to 0.362 +/- 0.047 mm2 (p < 0.05 vs. control rats) and from 2.000 +/- 0.136 to 1.374 +/- 0.180 (p < 0.05 vs. control rats). The vessel thrombosis rate after stent deployment was 30% in the control group and 11.1% in the treated group (p = NS). Moreover, the systemic administration of simvastatin did not affect hepatic and renal functions, blood pressure or heart rate. CONCLUSIONS: Simvastatin potently inhibits VSMC proliferation in vitro and reduces neointimal formation in a rat model of vascular injury.     

Abnormal blood-pressure response to exercise and oxygen consumption in patients with hypertrophic cardiomyopathy.

BACKGROUND: Abnormal blood-pressure response during exercise occurs in about one third of patients with hypertrophic cardiomyopathy (HCM), and it has been associated with a high risk of sudden cardiac death. We assessed the hemodynamics of exercise in HCM patients with abnormal blood-pressure response by using ambulatory radionuclide monitoring (VEST) of left-ventricular (LV) function, and exercise tolerance by oxygen consumption. METHODS: Twenty-two HCM patients underwent treadmill exercise during VEST monitoring. A cardiopulmonary exercise test was performed a few days after. The VEST data were averaged for 1 minute. Stroke volume, cardiac output, and systemic vascular resistance were expressed as percent of baseline. Exercise tolerance was assessed as maximal oxygen consumption. RESULTS: In eight HCM patients (36%) with an abnormal blood-pressure response, end-systolic volume increased more (52% +/- 21% vs 31% +/- 28%, P = .012), and the ejection fraction (-31% +/- 17% vs -14% +/- 22%, P = .029) and stroke volume (-21% +/- 21% vs 3% +/- 28%, P = .026) fell more, than in patients with normal response. Cardiac output increased less in the former patients (49% +/- 44% vs 94% +/- 44%, P = .012). Systemic vascular resistance decreased similarly, irrespective of blood-pressure response (-28% +/- 26% vs -34% +/- 26%, P = N.S.). Percent of maximal predicted oxygen consumption was lower in HCM patients with an abnormal blood-pressure response (63% +/- 11% vs 78% +/- 15%, P = .025). CONCLUSIONS: In HCM patients, abnormal blood-pressure response was associated with exercise-induced LV systolic dysfunction and impairment in oxygen consumption. This may cause hemodynamic instability, associated with a high risk of sudden cardiac death.