In-hospital management of elderly patients undergoing myocardial perfusion scintigraphy.

OBJECTIVE: To investigate the impact of myocardial perfusion scintigraphy results on the decision for invasive coronary angiography in elderly patients (≥75 years) with suspected coronary artery disease hospitalized in a single tertiary medical center. SUBJECTS AND METHODS: In the retrospective study, data of 276 (136 elderly) consecutive hospitalized patients referred to myocardial perfusion imaging were analyzed. The clinical characteristics, myocardial perfusion scintigraphy results, invasive coronary angiography and revascularization rates and in-hospital adverse events were identified by manually reviewing the patients' records. RESULTS: Ischemia was found in 40.2% of patients. There was no significant difference in the proportion of ischemia between elderly and younger patients (38.2% vs. 42.1%, P=0.508). Invasive coronary angiography was performed in 64.0% of patients with ischemia and in 6.8% of patients with normal myocardial perfusion imaging (P<0.001). The referral rate for invasive coronary angiography was not different between elderly and younger patients with ischemia (63.5% vs. 64.4%, P=0.848). Ischemia on myocardial perfusion imaging was the most predictive variable for a referral to invasive coronary angiography (odds ratio 31.8, 95% confidence interval 14.6-69.5, P<0.001). There was no significant difference between the younger and elderly patients in revascularization rate and adverse events until discharge (39% vs. 40%, P=0.99 and 7.1% vs. 8.8%, P=0.6, respectively). CONCLUSION: Ischemia on myocardial perfusion scintigraphy is a powerful predictor for in-hospital invasive coronary angiography independent of the patient's age. Elderly patients with ischemia received invasive coronary angiography equally as their younger counterparts and have similar rates of adverse events until discharge.

Determination of amputation level in ischaemic limbs using tcPO2 measurement.

BACKGROUND: Determination of the optimal amputation level is essential for patients, morbidity and rehabilitation. Various non-invasive procedures have been proposed to determine the optimal level of amputation. There is no consensus on the minimal tcPO2 level that is required to predict the healing of the stump. Therefore we aimed to rank the probability of primary wound healing at the most distal level and to answer the question if there is a lower limit of tcPO2 below which healing cannot occur. PATIENTS AND METHODS: 56 consecutive patients undergoing amputation below the knee for ischaemic gangrene of limbs were prospectively enrolled in the study. 39 were men (18 of whom were diabetics) and 17 women (8 diabetics) whose ages ranged from 45 to 87 years (mean 73 years). The total of 71 amputations was performed on the 56 patients: 39 below-knee with primary healing and, in 16 patients the above-knee reamputation was performed, due to the non-healing wound on the below-knee stump. The level of the amputation (below or above the knee) was in all cases decided solely on clinical grounds. TcPO2 was measured on each patient prior to amputation, on the dorsum of the foot and 10 cm below the knee. RESULTS: The median tcPO2 value on the dorsum of the foot of diseased legs before amputation was 12 mm Hg (range from 0 to 22 mm Hg). At the anticipated level of the amputation of the shank, the median value of tcPO2 was 28 mm Hg (8-56 mm Hg). Patients with primary healing of postoperative wounds had significantly higher values of tcPO2 than patients with fialure to heal (37 mm Hg; range 15-56 mm Hg vs. 18 mm Hg; range 8-36 mm Hg, p < 0.01). The success rate increased with higher tcPO2 values at the level of amputation. The 15% prevalence of reamputations was obtained for tcPO2 values between 25 and 36 mm Hg (median value 33 mm Hg) and the threshold value of tcPO2 below which the stump failed to heal was 15 mm Hg. CONCLUSIONS: Our study showed that tcPO2 is a reliable indicator of local ischemia. The integration of this parameter with other personal clinical criteria may be a valuable help to the surgeon in decision making.

Seasonal variation of some metabolic and haemostatic risk factors in subjects with and without coronary artery disease.

Acute myocardial infarction (AMI) is more frequent in winter months than in summer months. The aetiologic mechanisms underlying this seasonal pattern are poorly understood. We investigate whether seasonal variation of metabolic and haemostatic coronary risk factors exists, and whether this variation is more pronounced in subjects with coronary artery disease (CAD). In 82 subjects (47 free of clinical signs of CAD and in 35 survivors of AMI), measurements of body mass index (BMI), lipoproteins, glucose, insulin, plasminogen activator inhibitor-1, tissue-type plasminogen activator (t-PA), euglobulin clot lysis time, fibrinogen, and platelet count were performed twice in the cold months (December and March) and twice in the warm months (June and September). Significantly higher BMI (26.8 versus 26.2 kg/m2, P < 0.01), glucose (5.5 versus 5.1 mmol/l, P < 0.01), total cholesterol (5.61 versus 5.32 mmol/l, P < 0.05), low-density lipoprotein cholesterol (3.63 versus 3.34 mmol/l, P < 0.05), triglycerides (1.79 versus 1.61 mmol/l, P < 0.01), Lp(a) (270.7 versus 237.5 mg/l, P < 0.01), fibrinogen level (3.50 versus 2.95 g/l, P < 0.00001), platelet count (212 x 10(9) versus 173 x 10(9)/l, P < 0.01) and significantly lower high-density lipoprotein cholesterol level (1.22 versus 1.28 mmol/l, P < 0.05) were observed in the cold months compared with the warm months. Significant seasonal variation of t-PA activity (1.19 versus 0.87 IU/ml, P = 0.015) and t-PA antigen (8.5 versus 7.3 ng/ml, P = 0.05) was demonstrated only in subjects with CAD. Clustering of peak values of several metabolic and haemostatic coronary risk factors was observed in winter months. This variation might be of aetiopathogenetic importance for the seasonal pattern of acute myocardial infarction.

Fibrinolytic parameters and insulin resistance in young survivors of myocardial infarction with heterozygous familial hypercholesterolemia.

A characteristic feature of patients with heterozygous familial hypercholesterolemia (FH) is the premature occurrence of coronary artery disease because of elevated LDL cholesterol levels. Hyperinsulinemia and insulin resistance, important characteristics of the cardiovascular dysmetabolic syndrome (CDS), were found to be associated with coronary artery disease in FH subjects, as in the general population. We investigated whether hypofibrinolysis, as part of CDS, is independently associated with symptomatic coronary artery disease in these high-risk patients. Clinical examination (body mass index, waist circumference, blood pressure) and blood analysis (plasma tissue plasminogen activator (t-PA) antigen, plasminogen activator inhibitor (PAI-1) antigen and activity, fibrinogen, serum lipids and lipoproteins, fasting glucose and insulin) were carried out in 39 male patients with heterozygous FH (aged 46.6 +/- 8.8 years). Insulin resistance was calculated using the homeostasis model assessment (HOMA) mathematical model. Thirteen of the patients had suffered a myocardial infarction (MI) 5 to 8 years ago (aged 47.8 +/- 6.1 years) and 26 were free of coronary artery disease (aged 45.9 +/- 9.9 years). There was no difference in total and LDL cholesterol between the two groups. Patients with previous myocardial infarction had significantly higher levels of insulin, insulin resistance, triglycerides, t-PA antigen, PAI-1 antigen and activity, and significantly lower values of HDL cholesterol. Other widely recognised risk factors for coronary artery disease, such as smoking, systolic and diastolic blood pressure, obesity and age, did not differ significantly between the groups. In the logistic regression model, PAI-1 antigen, as a marker of hypofibrinolysis, emerged as an independent risk factor for the occurrence of myocardial infarction (odds ratio 1.55; p = 0.02). In summary our results suggest that the impairment of fibrinolytic activity resulting from elevated levels of PAI-1 antigen and activity and t-PA antigen is an independent variable in CDS associated with the premature occurrence of myocardial infarction in male patients with FH.

Combined hormone replacement therapy improves endothelial function in healthy postmenopausal women.

OBJECTIVES: Large scale epidemiological studies suggest that hormone replacement therapy (HRT) reduces cardiovascular events in postmenopausal women. Improvement in endothelial function may contribute to this protective effect. DESIGN: In a prospective, double blind study, 61 healthy postmenopausal women were randomized to receive either oral continuous combined HRT [oestradiol 2 mg and norethisterone acetate (NETA) 1 mg per day] or placebo. Endothelial function, assessed by flow-mediated vasodilation (FMD) of the brachial artery and expression of soluble endothelial cell adhesion molecules (CAM) were determined before, after 3 and 6 months of therapy. RESULTS: The FMD was significantly improved in women on combined HRT (from 5.97% to 10.94% after 3 months and to 10.58% after 6 months; both P < 0.01 versus baseline values) and did not change in the placebo group (6.92% at baseline, 5.86% after 3 and 6.26% after 6 months). After 3 months of combined HRT, significant decreases of 24.6% for E-selectin and 13.9% for intercellular adhesion molecule-1 (ICAM-1) were observed (both P < 0.01 versus baseline values) and were sustained after 6 months of therapy, whilst no differences emerged in the placebo group. CONCLUSIONS: Oestradiol and norethisterone acetate improve endothelial function by both enhancing FMD and reducing the levels of soluble E-selectin and ICAM-1 in healthy postmenopausal women.