{"id":45392,"date":"2014-10-01T16:58:47","date_gmt":"2014-10-01T20:58:47","guid":{"rendered":"http:\/\/blogs.nejm.org\/cardioexchange\/?post_type=discussion&p=45392"},"modified":"2014-10-23T06:46:24","modified_gmt":"2014-10-23T10:46:24","slug":"case-testosterone-replacement-therapy-and-cv-risk","status":"publish","type":"post","link":"https:\/\/blogs.nejm.org\/cardioexchange\/2014\/10\/01\/case-testosterone-replacement-therapy-and-cv-risk\/","title":{"rendered":"Case: Testosterone Replacement Therapy and CV Risk"},"content":{"rendered":"

A 47-year-old man presents to the hospital reporting 4 days of chest pain that occurs during treadmill exercise, left-arm and jaw discomfort, and shortness of breath with diaphoresis.<\/p>\n

His medical history is noteworthy only for orthopedic surgeries and use of testosterone replacement therapy for reportedly low testosterone syndrome.\u00a0He does not smoke and drinks alcohol only occasionally.\u00a0He works as a school administrator and a high school sports coach. He has no family history of coronary disease.<\/p>\n

The patient is obese, with a weight of 285 pounds and a body-mass index of 37 kg\/m2<\/sup>. His physical exam is otherwise unremarkable.<\/p>\n

His electrocardiogram is normal. Troponin I levels are 0.03, 0.04, and then 0.05 ng\/mL.<\/p>\n

The patient is transferred to a cardiac center for catheterization in the setting of acute coronary syndrome (ACS). Cardiac catheterization reveals normal LV function and an LV end-diastolic pressure of 8 mm Hg.\u00a0Coronary angiography shows a high-grade mid left anterior descending (LAD) stenosis, which is then successfully treated with a single drug-eluting stent.<\/p>\n

Before discharge, the patient has a total-cholesterol level of 184 mg\/dL, HDL of 29 mg\/dL, LDL of 101 mg\/dL, triglycerides of 270 mg\/dL, and fasting glucose of 87 mg\/dL. The patient is initiated on atorvastatin 80 mg and dual antiplatelet therapy, and he is discharged for follow-up.<\/p>\n

Angiograms of the LAD before and after PCI with a drug-eluting stent:<\/p>\n

\"pre<\/a><\/p>\n

\"post<\/a><\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

Questions:<\/b><\/p>\n

1. Did the testosterone replacement therapy play a major role, a minor but significant role (e.g., by amplifying other risk factors), or no role in this patient\u2019s atherothrombotic process?<\/p>\n

2. Is it safe to continue the testosterone replacement?<\/p>\n

3. According to the ACCF\/AHA risk estimator (which is not designed for use in secondary prevention), the patient\u2019s 10-year ASCVD risk before the ACS was 5.1%; therefore statin therapy would not have been recommended.\u00a0In secondary prevention, should we treat a patient who takes testosterone replacement differently than we treat a patient with multiple atherothrombotic risk factors or a higher risk according to the risk estimator?<\/p>\n

4. When the patient\u2019s risk is optimized, he loses weight, and he completes his dual antiplatelet therapy, could testosterone replacement be reinitiated safely (if it is stopped initially)?<\/p>\n

5. Does the patient need lifelong statin therapy?<\/p>\n

 <\/p>\n

Response:<\/strong><\/p>\n

Anna Catino, MD<\/a><\/p>\n

James Fang, MD<\/a><\/p>\n

October 7, 2014<\/p>\n

Questions:<\/strong><\/p>\n

1. Did the testosterone replacement therapy play a major role, a minor but significant role (e.g., by amplifying other risk factors), or no role in this patient\u2019s atherothrombotic process?<\/em><\/p>\n

Although observational data correlate low testosterone levels with CV risk, it remains to be seen whether treating low levels in the absence of symptomatic hypogonadism is beneficial. In fact, randomized trials of treatment for other reasons have suggested a signal of harm, particularly in patients with underlying CAD and the elderly. Therefore, a potential role for harm in this case could be made, despite the patient\u2019s age.<\/p>\n

2. Is it safe to continue the testosterone replacement?<\/em><\/p>\n

We would not continue testosterone therapy without unequivocal evidence of a symptomatic hypogonadal state, particularly in light of evidence of harm in recent randomized trials of testosterone supplementation.<\/p>\n

3. According to the ACCF\/AHA risk estimator (which is not designed for use in secondary prevention), the patient\u2019s 10-year ASCVD risk before the ACS was 5.1%; therefore statin therapy would not have been recommended. In secondary prevention, should we treat a patient who takes testosterone replacement differently than we treat a patient with multiple atherothrombotic risk factors or a higher risk according to the risk estimator?<\/em><\/p>\n

In secondary prevention, atherosclerosis is already present, so the priority is treatment of the atherosclerosis itself to reduce the morbidity and mortality of the disease. The use of testosterone replacement should be limited to treating patients with specific hypogonadal symptoms rather than modifying atherosclerosis disease progression. Otherwise, the secondary treatment should be no different than for other patients with known atherosclerosis.<\/p>\n

4. When the patient\u2019s risk is optimized, he loses weight, and he completes his dual antiplatelet therapy, could testosterone replacement be reinitiated safely (if it is stopped initially)?<\/em><\/p>\n

His testosterone levels should be re-assessed (two early morning levels, as recommended by endocrine societies) after significant weight loss. We suspect that this patient\u2019s testosterone levels will change and may even correct if his obesity were to be reversed. Low testosterone may simply reflect other CV risk factors or be driven by atherosclerosis itself (i.e., a risk marker rather than a risk factor). If his testosterone levels remained low, we would treat only in concert with an endocrinologist if a truly symptomatic hypogonadal state could be confirmed.<\/p>\n

5. Does the patient need lifelong statin therapy?<\/em><\/p>\n

Yes, given that he has atherosclerosis, which needs treatment independent of his testosterone status.<\/p>\n

 <\/p>\n

Wrap-Up:<\/b><\/p>\n

Seth Bilazarian, MD<\/a><\/p>\n

October 21, 2014<\/i><\/p>\n

The patient was discharged the day after his successful PCI. He was seen one week later by his clinical cardiologist, who recommended therapeutic lifestyle changes, continuation of dual antiplatelet therapy, and maintenance of statin therapy (atorvastatin 80 mg, once daily). Cardiac rehabilitation was recommended, but the patient declined. The patient was advised to discontinue the testosterone replacement therapy that he had started before his myocardial infarction.<\/p>\n

The table shows the patient\u2019s lipid values during his hospitalization (in March) and 3 months later (in June).<\/p>\n\n\n\n\n\n\n\n
<\/td>\n\n

March value<\/p>\n<\/td>\n

\n

June value<\/p>\n<\/td>\n<\/tr>\n

Total cholesterol (mg\/dL)<\/td>\n\n

163<\/p>\n<\/td>\n

\n

90<\/p>\n<\/td>\n<\/tr>\n

LDL cholesterol (mg\/dL)<\/td>\n\n

101<\/p>\n<\/td>\n

\n

43<\/p>\n<\/td>\n<\/tr>\n

HDL cholesterol (mg\/dL)<\/td>\n\n

27<\/p>\n<\/td>\n

\n

26<\/p>\n<\/td>\n<\/tr>\n

Triglycerides (mg\/dL)<\/td>\n\n

176<\/p>\n<\/td>\n

\n

103<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

The patient\u2019s weight fell from 285 pounds (BMI 37) to 251 pounds (BMI 34).<\/p>\n

Despite the recommendation to discontinue testosterone replacement therapy, the patient resumed it after discussion with his primary care provider, who had originally prescribed it. The PCP recommended that it be continued, given the lack of data on potential hazards and the symptom improvement it had yielded for the patient.<\/p>\n","protected":false},"excerpt":{"rendered":"

A 47-year-old man presents to the hospital reporting 4 days of chest pain that occurs during treadmill exercise, left-arm and jaw discomfort, and shortness of breath with diaphoresis. His medical history is noteworthy only for orthopedic surgeries and use of testosterone replacement therapy for reportedly low testosterone syndrome.\u00a0He does not smoke and drinks alcohol only […]<\/p>\n","protected":false},"author":574,"featured_media":0,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[9,7],"tags":[1566,1146,584,2044,2380],"class_list":["post-45392","post","type-post","status-publish","format-standard","hentry","category-interventional-cardiology","category-prevention","tag-acute-coronary-syndrome","tag-risk-calculators","tag-statins","tag-testosterone","tag-testosterone-replacement-therapy"],"_links":{"self":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts\/45392","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/users\/574"}],"replies":[{"embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/comments?post=45392"}],"version-history":[{"count":0,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts\/45392\/revisions"}],"wp:attachment":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/media?parent=45392"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/categories?post=45392"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/tags?post=45392"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}