madman
Super Moderator
Testosterone and the Heart | ECR Journal
Abstract
The development of a subnormal level of testosterone (T) is not universal in ageing men, with 75% of men retaining normal levels. However, a substantial number of men do develop T deficiency (TD), with many of them carrying a portfolio of cardiovascular (CV) risk factors, including type 2 diabetes (T2D) and the metabolic syndrome. TD increases the risk of CV disease (CVD) and the risk of developing T2D and the metabolic syndrome. The key symptoms suggesting low T are sexual in nature, including erectile dysfunction (ED), loss of night-time erections and reduced libido. Many men with heart disease, if asked, admit to ED being present; a problem that is often compounded by drugs used to treat CVD. A large number of studies and meta-analyses have provided evidence of the link between TD and an increase in CVD and total mortality. Patients with chronic heart failure (CHF) who have TD have a poor prognosis and this is associated with more frequent admissions and increased mortality compared with those who do not have TD. Conversely, in men with symptoms and documented TD, T therapy has been shown to have beneficial effects, namely improvement in exercise capacity in patients with CHF, improvement of myocardial ischaemia and coronary artery disease. Reductions in BMI and waist circumference, and improvements in glycaemic control and lipid profiles, are observed in T-deficient men receiving T therapy. These effects might be expected to translate into benefits and there are more than 100 studies showing CV benefit or improved CV risk factors with T therapy. There are flawed retrospective and prescribing data studies that have suggested increased mortality in treated men, which has led to regulatory warnings, and one placebo-controlled study demonstrating an increase in coronary artery non-calcified and total plaque volumes in men treated with T, which is open for debate. Men with ED and TD who fail to respond to phosphodiesterase type 5 (PDE5) inhibitors can be salvaged by treating the TD. There are data to suggest that T and PDE5 inhibitors may act synergistically to reduce CV risk.
Conclusion
The balance of evidence is that T therapy does not increase CV risk. Many studies have demonstrated that a low serum T concentration is associated with increased CV risk and mortality and that T therapy may have clinically relevant CV benefits.
Evidence demonstrates reduced CV risk with a higher endogenous T concentration, evidence of improvement of known CV risk factors with T therapy and reduced mortality in T deficient men who received T therapy versus untreated men, evidence of improvement of myocardial ischaemia in men with CAD, improved exercise capacity in men with CHF and improvement in serum glucose levels, HbA1c and insulin resistance in men with diabetes and prediabetes.
Bearing these facts in mind, when dealing with cardiac patients clinicians need to be alert to the possibility of undisclosed sexual problems and underlying TD, which are amenable to treatment.
The following statements are the conclusions of the BSSM:1
Abstract
The development of a subnormal level of testosterone (T) is not universal in ageing men, with 75% of men retaining normal levels. However, a substantial number of men do develop T deficiency (TD), with many of them carrying a portfolio of cardiovascular (CV) risk factors, including type 2 diabetes (T2D) and the metabolic syndrome. TD increases the risk of CV disease (CVD) and the risk of developing T2D and the metabolic syndrome. The key symptoms suggesting low T are sexual in nature, including erectile dysfunction (ED), loss of night-time erections and reduced libido. Many men with heart disease, if asked, admit to ED being present; a problem that is often compounded by drugs used to treat CVD. A large number of studies and meta-analyses have provided evidence of the link between TD and an increase in CVD and total mortality. Patients with chronic heart failure (CHF) who have TD have a poor prognosis and this is associated with more frequent admissions and increased mortality compared with those who do not have TD. Conversely, in men with symptoms and documented TD, T therapy has been shown to have beneficial effects, namely improvement in exercise capacity in patients with CHF, improvement of myocardial ischaemia and coronary artery disease. Reductions in BMI and waist circumference, and improvements in glycaemic control and lipid profiles, are observed in T-deficient men receiving T therapy. These effects might be expected to translate into benefits and there are more than 100 studies showing CV benefit or improved CV risk factors with T therapy. There are flawed retrospective and prescribing data studies that have suggested increased mortality in treated men, which has led to regulatory warnings, and one placebo-controlled study demonstrating an increase in coronary artery non-calcified and total plaque volumes in men treated with T, which is open for debate. Men with ED and TD who fail to respond to phosphodiesterase type 5 (PDE5) inhibitors can be salvaged by treating the TD. There are data to suggest that T and PDE5 inhibitors may act synergistically to reduce CV risk.
Conclusion
The balance of evidence is that T therapy does not increase CV risk. Many studies have demonstrated that a low serum T concentration is associated with increased CV risk and mortality and that T therapy may have clinically relevant CV benefits.
Evidence demonstrates reduced CV risk with a higher endogenous T concentration, evidence of improvement of known CV risk factors with T therapy and reduced mortality in T deficient men who received T therapy versus untreated men, evidence of improvement of myocardial ischaemia in men with CAD, improved exercise capacity in men with CHF and improvement in serum glucose levels, HbA1c and insulin resistance in men with diabetes and prediabetes.
Bearing these facts in mind, when dealing with cardiac patients clinicians need to be alert to the possibility of undisclosed sexual problems and underlying TD, which are amenable to treatment.
The following statements are the conclusions of the BSSM:1
- Other benefits of replacing T in deficient men are that beyond 6 months there is evidence of benefit of T therapy in terms of body composition, features of the metabolic syndrome and bone mineralization.
- T therapy also improves sexual desire, erectile function and sexual satisfaction. Reductions in BMI and waist circumference, and improvements in glycaemic control and lipid profiles, are observed in hypogonadal men receiving T therapy.
- Trials of T therapy should extend beyond 6 months and maximal benefit is often seen after 12 months.
- Patients should be informed about the benefits and side-effects of therapy to allow a joint decision regarding the appropriateness of treatment.
- The adverse effects of T therapy should be fully discussed and, where appropriate its potential effect on future fertility for each patient and his partner.
- When T therapy is prescribed, it should be accompanied by weight loss and lifestyle advice as standard management.
- For patients who are severely symptomatic, with T levels <8 nmol/l, dietary and lifestyle advice alone is unlikely to produce meaningful improvement within a relevant clinical period.
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