Coronary subclavian steal syndrome-is there a need for routine assessment for subclavian artery stenosis following coronary bypass surgery?

Subclavian artery stenosis (SAS) resulting in coronary subclavian steal syndrome (CSSS) is a common but under recognized pathology following coronary artery bypass surgery (CABG). Patients with SAS may be asymptomatic due to the sub-clinical diversion of blood flow from the myocardium and retrograde blood flow during catheter angiography in the left internal mammary artery (LIMA) may be the first suggestion of CSSS. The management of SAS, causing CSSS, may rarely require acute assessment and intervention. However, full anatomical assessment of the stenosis morphology may be limited on fluoroscopy. Correction of SAS may be essential to achieve effective reperfusion therapy.

Testosterone does not adversely affect fibrinogen or tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) levels in 46 men with chronic stable angina.

OBJECTIVE: In women, sex hormones cause increased morbidity and mortality in patients with coronary heart disease (CHD) and adversely affect the coagulation profile. We have studied the effect of physiological testosterone replacement therapy in men on coagulation factor expression, to determine if there is an increased risk of thrombosis. METHODS: Double-blind, randomized, placebo-controlled trial of testosterone in 46 men with chronic stable angina. Measurements of free, total and bioavailable testosterone, luteinising hormone (LH) and follicle-stimulating hormone (FSH), estradiol, plasminogen activator inhibitor-1 (PAI-1), fibrinogen, tissue plasminogen activator (tPA) and full blood count were made at 0, 6 and 14 weeks. RESULTS: Bioavailable testosterone levels were: 2.58 +/- 0.58 nmol/l at baseline, compared with 3.35 +/- 0.31 nmol/l at week 14 (P < 0.001) after treatment compared with 2.6 +/- 0.18 nmol/l and 2.44 +/- 0.18 nmol/l in the placebo group (P was not significant). There was no change in fibrinogen (3.03 +/- 0.18 g/l at baseline and 3.02 +/- 0.18 g/l at week 14, P = 0.24), tPA activity (26.77 +/- 4.9 Iu/ml and 25.67 +/- 4.4 Iu/ml, P = 0.88) or PAI-1 activity (0.49 +/- 0.85 Iu/ml and 0.36 +/- 0.06 Iu/ml, P = 0.16) with active treatment and no differences between the groups (at week 14, P value 0.98, 0.59 and 0.8 for fibrinogen, PAI-1 and tPA respectively). Haemoglobin concentration did not change over time, in the testosterone group (1.44 +/- 0.02 g/l and 1.45 +/- 0.02 g/l, P = 0.22). CONCLUSION: Physiological testosterone replacement does not adversely affect blood coagulation status.

Life-saving or life-prolonging? Interpreting trial data and survival curves for patients with congestive heart failure.

Chronic heart failure is responsible for considerable suffering and mortality throughout the world. Clinical trials have consistently demonstrated the benefits of pharmacological therapies such as angiotensin-converting enzyme inhibitors and beta-adrenoceptor blockers. These drugs are often quoted as reducing mortality from heart failure, yet all patients with heart failure deteriorate and most will die because of their disease. Therapies in heart failure are not truly life saving; they modify the natural history of the disease and delay the time to deterioration. The time benefit in survival is not usually reported in clinical trials, which are conducted over fixed time points and report risk reductions during this period only. In this paper, we discuss the use of prolongation of life statistics as an outcome measure in clinical trials and review simple techniques for calculating the lifetime benefit of pharmacological intervention in heart failure using data from a number of major studies

Testosterone as a protective factor against atherosclerosis--immunomodulation and influence upon plaque development and stability.

Inflammation plays a central pathogenic role in the initiation and progression of coronary atheroma and its clinical consequences. Cytokines are the mediators of cellular inflammation and promote local inflammation in the arterial wall, which may lead to vascular smooth muscle apoptosis, degradation of the fibrin cap and plaque rupture. Platelet adhesion and thrombus formation then occur, resulting clinically in unstable angina or myocardial infarction. Recent studies have suggested that cytokines are pathogenic, contributing directly to the disease process. 'Anti-cytokine' therapy may, therefore, be of benefit in preventing or slowing the progression of cardiovascular disease. Both oestrogens and testosterone have been shown to have immune-modulating effects; testosterone in particular appears to suppress activation of pro-inflammatory cytokines. Men with low testosterone levels are at increased risk of coronary artery disease. An anti-inflammatory effect of normal physiological levels of sex hormones may, therefore, be important in atheroprotection. In this Article, we discuss some of the mechanisms involved in atherosclerotic coronary artery disease and the putative link between testosterone deficiency and atheroma formation. We present the hypothesis that the immune-modulating properties of testosterone may be important in inhibiting atheroma formation and progression to acute coronary syndrome.

The Vanishing Stenosis: ST Elevation Myocardial Infarction and Rhythm Disturbance due to Coronary Artery Spasm-Case Report and Review of the Literature.

A 62-year-old lady was admitted with clinical and electrocardiograph features of acute myocardial infarction. Urgent coronary arteriography was performed, demonstrating a single discrete stenosis of one coronary artery. Following intracoronary injection of GTN, this stenosis completely resolved, as the symptoms did. The causes of acute myocardial infarction with normal coronary arteries are reviewed.

Androgens, insulin resistance and vascular disease in men.

Type 2 diabetes mellitus is increasing globally and is an established risk factor for the development of atherosclerotic vascular disease. Insulin resistance is the hallmark feature of type 2 diabetes and is also an important component of the metabolic syndrome. There is evidence to suggest that testosterone is an important regulator of insulin sensitivity in men. Observational studies have shown that testosterone levels are low in men with diabetes, visceral obesity (which is strongly associated with insulin resistance), coronary artery disease and metabolic syndrome. Short-term interventional studies have also demonstrated that testosterone replacement therapy produces an improvement in insulin sensitivity in men. Thus hypotestosteronaemia may have a role in the pathogenesis of insulin-resistant states and androgen replacement therapy could be a potential treatment that could be offered for improvements in glycaemic control and reduction in cardiovascular risk, particularly in diabetic men.

Testosterone replacement in hypogonadal men with angina improves ischaemic threshold and quality of life.

BACKGROUND: Low serum testosterone is associated with several cardiovascular risk factors including dyslipidaemia, adverse clotting profiles, obesity, and insulin resistance. Testosterone has been reported to improve symptoms of angina and delay time to ischaemic threshold in unselected men with coronary disease. OBJECTIVE: This randomised single blind placebo controlled crossover study compared testosterone replacement therapy (Sustanon 100) with placebo in 10 men with ischaemic heart disease and hypogonadism. RESULTS: Baseline total testosterone and bioavailable testosterone were respectively 4.2 (0.5) nmol/l and 1.7 (0.4) nmol/l. After a month of testosterone, delta value analysis between testosterone and placebo phase showed that mean (SD) trough testosterone concentrations increased significantly by 4.8 (6.6) nmol/l (total testosterone) (p = 0.05) and 3.8 (4.5) nmol/l (bioavailable testosterone) (p = 0.025), time to 1 mm ST segment depression assessed by Bruce protocol exercise treadmill testing increased by 74 (54) seconds (p = 0.002), and mood scores assessed with validated questionnaires all improved. Compared with placebo, testosterone therapy was also associated with a significant reduction of total cholesterol and serum tumour necrosis factor alpha with delta values of -0.41 (0.54) mmol/l (p = 0.04) and -1.8 (2.4) pg/ml (p = 0.05) respectively. CONCLUSION: Testosterone replacement therapy in hypogonadal men delays time to ischaemia, improves mood, and is associated with potentially beneficial reductions of total cholesterol and serum tumour necrosis factor alpha.