Does Testosterone Increase the Chance for a Heart Attack?

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Nelson Vergel

Nelson Vergel

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"Many healthcare providers hesitate to initiate men on testosterone replacement therapy (TRT) due to the belief that these treatments increase the risk of cardiovascular (CV) events. However, the data supporting this belief are conflicting. A systematic review and meta-analysis of 30 randomized trials assessed the effect of TRT on CV events and risk factors in 1642 men with different degrees of androgen deficiency were on TRT. The results were inconsistent across trials but did not support an association between testosterone use and important CV effects. In another systematic review and meta-analysis of 51 randomized trials, the relative risks of myocardial infarction, arrhythmia, coronary bypass surgery, and all-cause mortality were not significantly increased with TRT use.

The Testosterone in Older Men with Mobility Limitations (TOM) trial randomly assigned 209 men with mobility issues and low testosterone to 6 months' treatment with testosterone gel to improve lower extremity strength and physical function.


In this population of older men with limitations in mobility and a high prevalence of chronic disease, testosterone gel was associated with an increased risk of CV events. However, these results should be interpreted with caution, as the study was not designed to assess CV disease, and more patients in the testosterone arm had hypertension or dyslipidemia at baseline. Moreover, the prescribed dose of testosterone was two times the standard starting dose and the criteria for CV events were relatively subjective and non-specific, including for example the complaint of shortness of breath, tachycardia or leg edema. The small size of the trial and the unique population should limit physicians from making broader assumptions about the safety of TRT for other patient populations.

More recently, a retrospective study of 8709 hypogonadal men who underwent coronary angiography in the Veterans Affairs system between 2005 and 2011 assessed the association between testosterone therapy and all-cause mortality, myocardial infarction (MI) or stroke. Overall, the unadjusted data demonstrated a protective effect of TRT use on CV risk; however, the adjusted data showed an adverse impact. Puzzling, however, is that the testosterone levels among the men on TRT versus men not on TRT were unknown. The testosterone levels among the men experiencing a CV event versus men without an event were unknown. Also concerning is that about 100 of the “men” in this study were later reported to be women."

Source: Testosterone deficiency and replacement: Myths and Realities. Can Urol Assoc J 2014;8(7-8):S145-7.


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•An update on the role of testosterone replacement therapy in the management of hypogonadism

•A Review of Testosterone CV Studies Based on Prescription Data
 
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Defy Medical TRT clinic doctor
EMA Finds Little Evidence That Testosterone Ups CV Risk


"There is no consistent evidence that the use of testosterone in men with hypogonadism increases the risk for cardiovascular problems, according to a new review by the Pharmacovigilance Risk Assessment Committee (PRAC) of the European Medicines Agency (EMA).

The EMA launched this review regarding the cardiovascular risk for testosterone-containing medicines in April, following a similar announcement by the US Food and Drug Administration (FDA) earlier in the year.

Now the PRAC says the evidence concerning the risks of serious cardiovascular side effects with these medicines "is inconsistent." While some studies do suggest an increased risk for cardiac problems in men using testosterone compared with men not taking it, these had some limitations, and other studies did not confirm this risk.

The committee has determined that the benefits of testosterone continue to outweigh its risks but stresses that testosterone-containing medicines should be used only where lack of testosterone has been confirmed by signs and symptoms as well as laboratory tests."

http://www.medscape.com/viewarticle/833079
 
European Medicines Agency's (EMA) Pharmacovigilance Risk Assessment Committee (PRAC) Review Does Not Confirm Increase in Heart Problems with Testosterone Medicines
http://goo.gl/7VK9BW

The EMA's Pharmacovigilance Risk Assessment Committee (PRAC) has completed an EU-wide review of testosterone-containing medicines following concerns over serious side effects on the heart and blood vessels, including heart attack.

The PRAC review did not find consistent evidence that the use of testosterone in men who do not produce enough testosterone (a condition known as hypogonadism) increases the risk of heart problems.

The committee considered that the benefits of testosterone continue to outweigh its risks but recommended that testosterone-containing medicines should only be used where lack of testosterone has been confirmed by signs and symptoms as well as laboratory tests.

The evidence about the risks of serious side effects on the heart of these medicines is inconsistent. While some studies including three recently published studies did suggest an increased risk of heart problems in men using testosterone compared with men not taking it, these studies had some limitations and others did not confirm this risk.

The PRAC also noted that the lack of testosterone itself could increase the risk of heart problems.

The PRAC therefore recommended that testosterone-containing medicines should only be used if the lack of testosterone has been confirmed by signs and symptoms as well as laboratory tests. The EU product information for all testosterone-containing medicines should be updated to include this recommendation as well as warnings against use in men suffering from severe heart, liver or kidney problems.

The limited data on safety and effectiveness in patients over 65 years of age as well as the fact that testosterone levels decrease with age and that age-specific testosterone reference values do not exist will be highlighted in the product information.

The safety of testosterone medicines should continue to be monitored. In particular, a number of studies are still ongoing and their results will be considered in future regular benefit-risk assessments for these medicines.
 
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This is a great table that compares different studies that used testosterone gels, injections, patches or oral. They compared the relative risk for cardiovascular risk and found injections to be the safest testosterone replacement method.


Am J Physiol Endocrinol Metab. 2015 Apr 21:ajpendo.00111.2015. doi: 10.1152/ajpendo.00111.2015. [Epub ahead of print]

Injection of Testosterone May be Safer and More effective than Transdermal Administration for combating Loss of Muscle and Bone in Older Men.

Borst SE, Yarrow JF.
TRT heart studies.jpg
 
Here is a review that contradicts the previously posted one.

Comparative Safety of Testosterone Dosage Forms

Importance Increases in testosterone use and mixed reports of adverse events have raised concerns about the cardiovascular safety of testosterone. Testosterone is available in several delivery mechanisms with varying pharmacokinetics; injections cause spikes in testosterone levels, and transdermal patches and gels cause more subtle but sustained increases. The comparative cardiovascular safety of gels, injections, and patches has not been studied.

Objective To determine the comparative cardiovascular safety of testosterone injections, patches, and gels.

Design, Setting, and Participants A retrospective cohort study was conducted using administrative claims from a commercially insured (January 1, 2000, to December 31, 2012) and Medicare (January 1, 2007, to December 31, 2010) population in the United States and general practitioner records from the United Kingdom (January 1, 2000, to June 30, 2012). Participants included 13 men (aged ≥18 years) who initiated use of testosterone patches, gels, or 14 injections following 180 days with no testosterone use. Our analysis was conducted from December 11, 2013, to November 12, 2014.

Exposures New initiation of a testosterone dosage form, with use monitored for up to 1 year.

Main Outcomes and Measures Inpatient or outpatient medical records, diagnoses, or claims for cardiovascular and cerebrovascular events including myocardial infarction (MI), unstable angina, stroke, and composite acute event (MI, unstable angina, or stroke); venous thromboembolism (VTE); mortality; and all-cause hospitalization.

Results We identified 544,115 testosterone initiators between the 3 data sets: 37.4% injection, 6.9% patch, and 55.8% gel. The majority of men in the Medicare cohort were injection initiators (51.2%), most in the US commercially insured population were gel initiators (56.5%), and the UK database included equal proportions of injections and gel users (approximately 41%). With analysis conducted using hazard ratios and 95% CIs, compared with men using gels, injection initiators had higher hazards of cardiovascular events (ie, MI, unstable angina, and stroke) (1.26; 1.18-1.35), hospitalization (1.16; 1.13-1.19), and death (1.34; 1.15-1.56) but not VTE (0.92; 0.76-1.11). Compared with gels, patches did not confer increased hazards of cardiovascular events (1.10; 0.94-1.29), hospitalization (1.04; 1.00-1.08), death (1.02; 0.77-1.33), or VTE (1.08; 0.79-1.47).

Conclusions and Relevance Testosterone injections were associated with a greater risk of cardiovascular events, hospitalizations, and deaths compared with gels. Patches and gels had similar risk profiles. However, this study did not assess whether patients met criteria for use of testosterone and did not assess the safety of testosterone among users compared with nonusers of the drug.

JAMA Intern Med. Published online May 11, 2015.
 
Low serum testosterone level was associated with extensive coronary artery calcification in elderly male patients with stable coronary artery disease.

Lai J, et al. Coron Artery Dis. 2015.


Abstract

BACKGROUND: Coronary artery calcification (CAC) is a pandemic condition in elderly patients with coronary artery disease (CAD) and associated with a worse prognosis. Although available data have shown an association between testosterone levels in men and CAD, the association between testosterone and CAC in elderly male patients with CAD remains unknown.

METHODS: A total of 211 consecutive male patients (age≥65 years) who underwent first multidetector computed tomography and following angiography were enrolled from our institution between March 2009 and September 2014. CAD was angiographically documented as significant stenoses (reduction≥50% of the lumen diameter) on any major coronary vessel. The standard Agatston calcium score was calculated. The relationship of serum testosterone level with the CAC score measured by multidetector computed tomography in elderly male patients with stable CAD was evaluated. For data analyses, the CAC score was divided into four categories: 11-99, 100-399, and 400, corresponding to minimal, moderate, increased, and extensive calcification.

RESULTS: Patients with higher CAC scores had significantly lower testosterone levels than patients with lower CAC scores (P=0.048). In logistic regression analysis, testosterone level remained an independent predictor of extensive CAC (odds ratio 0.997, 95% confidence interval 0.994-0.999, P=0.043).

CONCLUSION: Our findings indicate an inverse association between testosterone level and the susceptibility to extensive CAC in elderly men with stable CAD.
 
Does Testosterone Replacement Increase Cardiovascular Risks?

A meta-analysis with a database spanning 1981–2008 evaluated men with low or low-normal testosterone treated with testosterone for at least 90 days (23). The aim was to evaluate the adverse effects of testosterone therapy in men. Fifty-one testosterone therapy trials, ranging in duration from 3 months to 3 years, were included. There was no increase in the rates of death, myocardial infarction (MI), revascularization procedures, or cardiac arrhythmias as compared with the placebo-nonintervention groups. None of these trials, however, was powered to show a difference in these end points.


On the other hand, a number of recent studies have reported increased cardiovascular events and mortality in testosterone-treated men. In the Testosterone in Older Men with Mobility Limitations trial, 209 elderly frail men, mean age 74 years, with limitations in mobility and low total serum testosterone levels, were randomly assigned a placebo gel or testosterone gel, to be applied daily for 6 months (24). There was a high prevalence of comorbidities, including hypertension, diabetes, congestive heart failure, and renal insufficiency. A total of 23 subjects in the testosterone group, as compared with 5 in the placebo group, had cardiovascular-related adverse events, including 1 death in the treatment group. The study was halted because of these adverse effects. It should be noted, however, that the study was not designed to investigate cardiovascular events and no criteria for defining cardiovascular events were set out in advance. The majority of events would not be included as an “event” in any cardiovascular study due to questionable clinical significance, including peripheral edema, hypertension, and tachycardia, as well as nonspecific electrocardiogram changes. With a low number of serious events and the absence of any predetermined cardiovascular end points or specific cardiovascular investigations, this study does not demonstrate a clear increased cardiovascular disease risk. However, it raises concerns that testosterone treatment could increase cardiovascular events in men with pre-existing cardiovascular disease. Other studies in elderly populations also have not shown an increase in cardiac events after testosterone replacement (25–29). A prospective, randomized, double-blind multicenter trial of transdermal testosterone therapy for 1 year in 220 hypogonadal men with type 2 diabetes or metabolic syndrome reported that cardiovascular events were less common with testosterone therapy than with placebo (4.6% versus 10.7%), but this difference was not statistically significant (P = .095) (18). A recent 6-month randomized, placebo-controlled trial of intramuscular testosterone therapy in 88 men with type 2 diabetes did not show a difference in rates of cardiovascular events amongst testosterone or placebo groups (30).

Five meta-analyses have evaluated the effect of testosterone therapy on cardiovascular events (23,31–34). Of these, only one reported increased cardiovascular events with testosterone therapy versus placebo (33). This study, by Xu et al (33), evaluated 27 randomized controlled trials, each at least 3 months in duration. The authors concluded that testosterone therapy increased the risk of “cardiovascular related events” by 54%. However, “events” again included clinically questionably anecdotal items, including peripheral edema and hypertension. On the contrary, a recent meta-analysis that included 75 randomized, placebo-controlled trials of testosterone treatment and evaluated the incidence of major adverse cardiovascular events did not find any association of testosterone therapy with actual cardiovascular events. (34).

It should be emphasized that none of these trials was designed to assess cardiovascular events. Randomized controlled trials designed to evaluate the effect of testosterone replacement in men on cardiovascular events or mortality have not yet been carried out. At this time, there is clearly a paucity of long-term studies to carry out a meta-analysis of the relationship of testosterone therapy with actual cardiovascular events.

Two retrospective studies have shown a benefit of testosterone treatment on cardiovascular events. An observational cohort study examined total mortality rates in 398 hypogonadal men (total testosterone <250 ng/dL) treated with testosterone therapy at 7 Veteran Affairs hospitals in the northwest United States (35). A total of 633 untreated hypogonadal men served as the comparison group. The mean age was 62 years, and the mean follow-up period was 40 months. Mortality rates in treated and untreated men were 10 and 21% (P<.001), respectively. After multifactorial adjustment, testosterone-treated men had a 39% reduction in mortality risk (P = .008). A retrospective cohort study in an endocrine clinic investigated the effect of TRT in 238 hypogonadal men with type 2 diabetes on all-cause mortality (36). Sixty-four men received testosterone (mean duration, 42 ± 21 months). A total of 60 patients received TRT for 12 months or more and 51 had treatment for 2 years or more. A total of 174 men were not treated. The mortality rate in the untreated group was 20%, whereas the group treated with testosterone had a mortality rate of 9.4% (P = .002). After multivariable adjustment, the hazard ratio for decreased survival in the untreated group was 2.3 (95% confidence interval [CI], 1.3 to 3.9; P = .004). By comparison, the mortality rate in a cohort of 343 men with type 2 diabetes and normal testosterone concentrations was 9% (36). Although this study showed a reduction in cardiovascular risk after testosterone, this study was retrospective. While of interest, retrospective studies should serve as hypothesis generating for randomized clinical trials and cannot serve as the basis for drawing firm conclusions regarding therapy.

Two recent publications have raised concern that testosterone therapy increases cardiovascular risk (1,2). These studies were retrospective observational analyses and have been criticized, based on detailed epidemiologic and statistical analyses (37,38). One study examined mortality, MI, and stroke rates in men with low testosterone levels (<300 ng/mL) who had undergone coronary angiography (1). The published critiques have focused on many flaws in this study, among which are:
Actual reported rate of events was 10.1% for the testosterone-treated group and 21.2% in controls, showing a reduced event rate in the treated group by more than 50% (38,39). The Kaplan-Meier calculation based on statistical adjustment for more than 50 variables converted this into an event rate of 19.9% in the untreated group and 25.7% in the testosterone-therapy group at 3 years, thus reversing the results of raw data. The risk differences were 1.3% (95% CI, −7.1 to 9.7%) at 1 year, 3.1% (95% CI, −4.9 to 11.0%) at 2 years, and 5.8% (95% CI, −1.4 to 13.1%) at 3 years. While these were not statistically significant, the reported overall Kaplan-Meier survival curve based on these estimates over 3 years suggested a hazard ratio of 1.29 (95% CI, 1.04 to 1.58; P = .02).

Statistical adjustments were done for over 50 variables, but not were done for baseline testosterone concentrations. This is an important lapse, since the patients in the testosterone-therapy group had lower baseline testosterone concentrations than the untreated group (175.5 ng/dL versus 206.5 ng/dL; P<.001) and since testosterone concentrations are inversely related to mortality in elderly men (3).

The mean duration of therapy was only 1 year. Men receiving testosterone therapy had limited follow-up. There was no information about whether subjects in the testosterone arm of the study actually took testosterone. Moreover, 40% did not have follow-up testosterone measurements during testosterone therapy. Of the 60% who had posttreatment testosterone concentration measured, the mean concentration increased from 175.5 ng/dL to only 332.2 ng/dL, evidently due to inadequate replacement (7,40,41). The fact that complex statistical adjustments reversed the conclusions of the raw data likely point to the importance of comorbidities in predicting cardiovascular events, rather than that of testosterone therapy.

This study has undergone 2 published corrections. The first was for misreporting their results as “absolute risk” when in fact the results were based on highly statistical, derived estimates and, as noted above, were not supported by the raw data. A second correction was published 4 months after publication, when the authors admitted to a series of data errors. To date, 29 medical societies have called for retraction of this article based on the conclusion that the reported results represent “misinformation” (42).

The second study, by Finkle et al (2), examined 55,593 insurance claims with the information based on diagnosis codes, procedure codes, and prescription data. No data were available on indications for testosterone therapy prescription, race, laboratory findings, occupational, environmental, or lifestyle factors. They reported an increased rate of nonfatal MIs (from 0.35 to 0.48%; rate ratio, 1.36; 95% CI, 1.03 to 1.81) within the first 90 days of filling the testosterone prescription compared with the previous 12 months. However, since this was a retrospective study and not a prospective one, it is critical to understand that the population was preselected based on potentially requiring testosterone and thus being hypogonadal and having a relatively higher cardiovascular risk. There was no control group of untreated hypogonadal patients. Furthermore, there were no data on testosterone concentrations prior to or following testosterone treatment. Nor were any data available on the diagnosis, blood pressure, smoking, or body mass index. The “lead-in” period of 12 months prior to the prescription of testosterone does not represent an adequate control, especially in view of an increase of 36% within 90 days of testosterone use, which seems highly improbable in view of other studies with testosterone replacement.

AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY POSITION STATEMENT ON THE ASSOCIATION OF TESTOSTERONE AND CARDIOVASCULAR RISK
 
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Five meta-analyses have evaluated the effect of testosterone therapy on cardiovascular events (23,31–34). Of these, only one reported increased cardiovascular events with testosterone therapy versus placebo (33). This study, by Xu et al (33), evaluated 27 randomized controlled trials, each at least 3 months in duration. The authors concluded that testosterone therapy increased the risk of “cardiovascular related events” by 54%. However, “events” again included clinically questionably anecdotal items, including peripheral edema and hypertension. On the contrary, a recent meta-analysis that included 75 randomized, placebo-controlled trials of testosterone treatment and evaluated the incidence of major adverse cardiovascular events did not find any association of testosterone therapy with actual cardiovascular events. (34).


It should be emphasized that none of these trials was designed to assess cardiovascular events. Randomized controlled trials designed to evaluate the effect of testosterone replacement in men on cardiovascular events or mortality have not yet been carried out. At this time, there is clearly a paucity of long-term studies to carry out a meta-analysis of the relationship of testosterone therapy with actual cardiovascular events.

Two retrospective studies have shown a benefit of testosterone treatment on cardiovascular events. An observational cohort study examined total mortality rates in 398 hypogonadal men (total testosterone <250 ng/dL) treated with testosterone therapy at 7 Veteran Affairs hospitals in the northwest United States (35). A total of 633 untreated hypogonadal men served as the comparison group. The mean age was 62 years, and the mean follow-up period was 40 months. Mortality rates in treated and untreated men were 10 and 21% (P<.001), respectively. After multifactorial adjustment, testosterone-treated men had a 39% reduction in mortality risk (P = .008). A retrospective cohort study in an endocrine clinic investigated the effect of TRT in 238 hypogonadal men with type 2 diabetes on all-cause mortality (36). Sixty-four men received testosterone (mean duration, 42 ± 21 months). A total of 60 patients received TRT for 12 months or more and 51 had treatment for 2 years or more. A total of 174 men were not treated. The mortality rate in the untreated group was 20%, whereas the group treated with testosterone had a mortality rate of 9.4% (P = .002). After multivariable adjustment, the hazard ratio for decreased survival in the untreated group was 2.3 (95% confidence interval [CI], 1.3 to 3.9; P = .004). By comparison, the mortality rate in a cohort of 343 men with type 2 diabetes and normal testosterone concentrations was 9% (36). Although this study showed a reduction in cardiovascular risk after testosterone, this study was retrospective. While of interest, retrospective studies should serve as hypothesis generating for randomized clinical trials and cannot serve as the basis for drawing firm conclusions regarding therapy.

Two recent publications have raised concern that testosterone therapy increases cardiovascular risk (1,2). These studies were retrospective observational analyses and have been criticized, based on detailed epidemiologic and statistical analyses (37,38). One study examined mortality, MI, and stroke rates in men with low testosterone levels (<300 ng/mL) who had undergone coronary angiography (1). The published critiques have focused on many flaws in this study, among which are:

Actual reported rate of events was 10.1% for the testosterone-treated group and 21.2% in controls, showing a reduced event rate in the treated group by more than 50% (38,39). The Kaplan-Meier calculation based on statistical adjustment for more than 50 variables converted this into an event rate of 19.9% in the untreated group and 25.7% in the testosterone-therapy group at 3 years, thus reversing the results of raw data. The risk differences were 1.3% (95% CI, −7.1 to 9.7%) at 1 year, 3.1% (95% CI, −4.9 to 11.0%) at 2 years, and 5.8% (95% CI, −1.4 to 13.1%) at 3 years. While these were not statistically significant, the reported overall Kaplan-Meier survival curve based on these estimates over 3 years suggested a hazard ratio of 1.29 (95% CI, 1.04 to 1.58; P = .02).

Statistical adjustments were done for over 50 variables, but not were done for baseline testosterone concentrations. This is an important lapse, since the patients in the testosterone-therapy group had lower baseline testosterone concentrations than the untreated group (175.5 ng/dL versus 206.5 ng/dL; P<.001) and since testosterone concentrations are inversely related to mortality in elderly men (3).

The mean duration of therapy was only 1 year. Men receiving testosterone therapy had limited follow-up. There was no information about whether subjects in the testosterone arm of the study actually took testosterone. Moreover, 40% did not have follow-up testosterone measurements during testosterone therapy. Of the 60% who had posttreatment testosterone concentration measured, the mean concentration increased from 175.5 ng/dL to only 332.2 ng/dL, evidently due to inadequate replacement (7,40,41). The fact that complex statistical adjustments reversed the conclusions of the raw data likely point to the importance of comorbidities in predicting cardiovascular events, rather than that of testosterone therapy.
This study has undergone 2 published corrections. The first was for misreporting their results as “absolute risk” when in fact the results were based on highly statistical, derived estimates and, as noted above, were not supported by the raw data. A second correction was published 4 months after publication, when the authors admitted to a series of data errors. To date, 29 medical societies have called for retraction of this article based on the conclusion that the reported results represent “misinformation” (42).

The second study, by Finkle et al (2), examined 55,593 insurance claims with the information based on diagnosis codes, procedure codes, and prescription data. No data were available on indications for testosterone therapy prescription, race, laboratory findings, occupational, environmental, or lifestyle factors. They reported an increased rate of nonfatal MIs (from 0.35 to 0.48%; rate ratio, 1.36; 95% CI, 1.03 to 1.81) within the first 90 days of filling the testosterone prescription compared with the previous 12 months. However, since this was a retrospective study and not a prospective one, it is critical to understand that the population was preselected based on potentially requiring testosterone and thus being hypogonadal and having a relatively higher cardiovascular risk. There was no control group of untreated hypogonadal patients. Furthermore, there were no data on testosterone concentrations prior to or following testosterone treatment. Nor were any data available on the diagnosis, blood pressure, smoking, or body mass index. The “lead-in” period of 12 months prior to the prescription of testosterone does not represent an adequate control, especially in view of an increase of 36% within 90 days of testosterone use, which seems highly improbable in view of other studies with testosterone replacement.

In contrast, another retrospective claims-based analysis did not find an association of testosterone treatment with MI (6). This recently published retrospective cohort study used enrollment and claims data for a 5% national sample of Medicare beneficiaries. The authors compared 6,355 men aged 66 years or older who received intramuscular testosterone treatment to 19,065 controls. The primary outcome was MI based on discharge diagnosis ICD-9 code. After adjusting for demographic and clinical characteristics, testosterone therapy was not associated with an increased risk of MI (hazard ratio, 0.84; 95% CI, 0.69 to 1.02). Furthermore, testosterone therapy seemed to be protective in men at highest risk of MI (hazard ratio, 0.69; 95% CI, 0.53 to 0.92). However, being a retrospective claims-based analysis, this study also has the limitations mentioned above.


Full paper
 
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Testosterone Replacement Therapy and Cardiovascular Risk: A Review


Recent reports in the scientific and lay press have suggested that testosterone (T) replacement therapy (TRT) is likely to increase cardiovascular (CV) risk.

In a final report released in 2015, the Food and Drug Administration (FDA) cautioned that prescribing T products is approved only for men who have low T levels due to primary or secondary hypogonadism resulting from problems within the testis, pituitary, or hypothalamus (e.g., genetic problems or damage from surgery, chemotherapy, or infection).

In this report, the FDA emphasized that the benefits and safety of T medications have not been established for the treatment of low T levels due to aging, even if a man's symptoms seem to be related to low T.

In this paper, we reviewed the available evidence on the association between TRT and CV risk.

In particular, data from randomized controlled studies and information derived from observational and pharmacoepidemiological investigations were scrutinized.
The data meta-analyzed here do not support any causal role between TRT and adverse CV events. This is especially true when hypogonadism is properly diagnosed and replacement therapy is correctly performed.

Elevated hematocrit represents the most common adverse event related to TRT. Hence, it is important to monitor hematocrit at regular intervals in T-treated subjects in order to avoid potentially serious adverse events.

Corona GG, Rastrelli G, Maseroli E, Sforza A, Maggi M. Testosterone Replacement Therapy and Cardiovascular Risk: A Review. World J Mens Health 2015;33(3):130-42.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4709428/
 
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