Erectile dysfunction is associated with higher cardiovascular risk and all cause mortality
February 20, 2013
Cardiovascular (CV) disease and erectile dysfunction (ED) share common risk factors, whereas evidence-based studies have identified pathophysiological links as endothelial dysfunction and inflammation. Thus, identifying ED may be a useful predictor of future CV events.
Vlachopoulos et al. (1) performed the meta-analysis of 14 studies including jointly 92757 men (various outcomes have not necessarily been studied in all men). Total CV events were defined as CV death, myocardial infarction, revascularization, cerebrovascular events (stroke, transient ischemic attacks, intracranial hemorrhage), peripheral vascular disease, angina, heart failure and arrhythmia. ED was associated with a significantly higher (by 44%) risk of total CV events. The risk was significantly increased in the intermediate-risk group (by 51%) and in the high-risk group (by 30%), but not in the low-risk group. In an analysis performed in the studies in which the analyses were adjusted for main CV confounders, the increase in the risk of total CV event associated with ED was similar to the overall combined estimated risk. It shows that the higher CV risk in men with ED was independent of their higher baseline CV risk. The increase in the CV risk associated with ED was higher in studies in which ED was diagnosed with a validated questionnaire (by 61%) compared with a single question (by 27%).
ED was also associated with a significantly higher risk of myocardial infarction (by 62%) and of cerebrovascular event (by 39%). ED was associated with a significantly higher all-cause mortality (by 25%), mainly in men with known CV disease, but not with CV mortality. The findings of the meta-analyses were not related to the publication bias. Finally, meta-regression analyses showed that ED was predictive of CV events mainly in younger men, smokers as well as in men with higher total cholesterol and lower HDL-cholesterol levels.
Thus, screening and diagnosing ED can be important for primary prevention in the clinical practice because ED assessment offers an easy, low-cost alternative for CV biomarkers. The risk conferred by ED on the CV events is of a magnitude similar to that of the risk conferred by established risk predictors such as hypertension or dyslipidemia. ED can describe the CV risk particularly in men belonging to the intermediate-risk category. This group requires further risk reclassification and ED may be an additional predictor permitting to better assess the individual CV risk. Furthermore, the use of a validated questionnaire improves the diagnosis of ED and provides a stronger association between ED and the CV risk.
Overall these findings show that the assessment of ED using a validated method may help to estimate the CV risk in the clinical practice.
Reference: Vlachopoulos CV, Terentes-Printzios DG, Ioakeimidis NK, Aznaouridis KA, Stefanadis CI. Prediction of cardiovascular events and all-cause mortality with erectile dysfunction: a systematic review and meta-analysis of cohort studies. Circ Cardiovasc Qual Outcomes. 2013 6:99-109.
Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline
September 29, 2012
Hypertriglyceridemia is a known risk factor for both cardiovascular disease and pancreatitis. The National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III Guidelines from 2001 have recommended screening adults for hypertriglyceridemia as part of a fasting lipid panel at least once every 5 years. A recent Endocrine Society Task Force convened to review existing guidelines for evaluation and treatment of hypertriglyceridemia.
The Task Force recommends the following:
- Diagnosis of hypertriglyceridemia should be based upon fasting triglyceride levels
- Measurement of aoplipoprotein B or lipoprotein (a) may be of value
- Patients with elevated fasting triglycerides should be evaluated for secondary causes of hyperlipidemia including endocrine conditions and medications
- Patients with primary hypertriglyceridemia should be evaluated for additional cardiovascular risk factors including central obesity, hypertension, impaired glucose metabolism, and liver dysfunction
- Patients with primary hypertriglyceridemia should be evaluated for a family history of dyslipidemia and cardiovascular disease to assess genetic causes as well as future risk
- Lifestyle therapy, including dietary counseling and physical activity, should be promoted to achieve weight reduction in obese patients
- For severe hypertriglyceridemia (> 1000mg/dl), pharmacotherapy should be prescribed along with dietary fat and simple carbohydrate reduction to reduce the risk of pancreatitis
- Fibrates should be used as first-line agents for reduction of triglycerides in patients at risk for triglyceride-induced pancreatitis
- Fibrates, niacin, and α-3 fatty acids alone or in combination with statins should be considered as treatment options in patients with moderate to severe hypertriglyceridemia
- Statins should not be used as monotherapy for severe or very severe hypertriglyceridemia, but may be used for treatment of moderate hypertriglyceridemia when indicated to modify cardiovascular risk
Reference: Berglund L, Brunzell JD, Goldberg AC, et al. Evaluation and treatment of hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline
2012 Updated ACCF/AHA Guidelines for Unstable Angina and Non-ST-Elevation Myocardial Infarction
August 21, 2012
Recent guideline updates for unstable angina (UA) and non-ST-elevation myocardial infarction (NSTEMI) recommend the following:
- Aspirin should be administered to UA/NSTEMI patients as soon as possible after hospital presentation and continued indefinitely to patients who do not have contraindications
- A loading dose followed by daily maintenance dose of either clopidogrel, prasurgel, or ticagrelor should be administered to UA/NSTEMI patients who are unable to take aspirin
- After cardiovascular stress testing, the patient is classified as:
- Not at low risk, diagnostic angiography should be performed
- At low risk, continue aspirin indefinitely, continue clopidogrel or ticagrelor for up to 12 months, continue unfractionated heparin for 48 hours
- For UA/NSTEMI patients in who coronary artery bypass grafting (CABG) is selected as a postangiography management strategy, continue aspirin and unfractionated heparin
- Diagnostic angiography with intent to perform revascularization is indicated in initially stabilized UA/NSTEMI patients without serious comorbities who have an elevated risk for clinical events
- It is reasonable to choose an early invasive strategy (within 12 to 24 hours of admission) over a delayed invasive strategy for initially stabilized high-risk patients with UA/NSTEMI
- For UA/NSTEMI patients treated with a stent, aspirin should be continued indefinitely with clopidogrel 75mg daily, prasurgel 10mg daily or ticagrelor 90mg twice daily for at least 12 months in patients receiving a drug-eluting stent
- Medical treatment in acute phase of UA/NSTEMI and decisions on whether to perform stress testing, angiography, and revascularization should be similar in patients with or without diabetes
- Creatinine clearance should be estimated in patients with UA/NSTEMI and the doses of renally-cleared medications should be adjusted according to the pharmacokinetics of specific medications
Reference: Jneid H, Anderson JL, Wright RS, et al. 2012 ACCF/AHA Focused Update of the Guideline for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction (Updating the 2007 Guideline and Replacing the 2011 Focused Update). Circulation 2012;126:875-910.
A Tale of Coronary Artery Disease and Myocardial Infarction
June 25, 2012
Cardiovascular disease remains the leading cause of death amongst men world-wide. In a commemorative 200th anniversary article of the New England Journal of Medicine, Nabel and Braunwald review the medical discoveries regarding diagnosis and treatment of coronary artery disease (CAD) and myocardial infarction (MI)) over the past two centuries. “Remarks on Angina Pectoris” by John Warren, M.D. appeared as the first article in the first issue of The New England Journal of Medicine and Surgery in 1812. At that time, little was known about the pathogenesis of the disease. Treatment consisted primarily of bloodletting, opium analgesia, and bed rest. It was not until the end of the 19th century that scientists discovered that blockage of coronary arteries caused the clinical sequelae of CAD. Physiologists observed that ligating the coronary artery of a dog quickly resulted in death. In 1929, Werner Forssman performed the first human cardiac catheterization study– on himself. Despite a better understanding of the disease, bed rest remained the standard treatment for patents who presented with acute MI until the mid-20th century.
In response to the alarming number of apparently healthy men who were dying suddenly of MI, the National Heart Institute established the Framingham Heart Study in 1948. Analysis of lifestyles of the enrollees revealed the breakthrough discovery that elevated blood pressure and cholesterol levels were associated with increased incidence of CAD. Large scale educational campaigns which addressed these risk factors soon followed, and resulted in a decline in age-adjusted cardiac death rates. In 1961, the incarnation of the coronary care unit (CCU), which provided continuous cardiac monitoring and external defibrillation, dramatically reduced in-hospital mortality of patients admitted with acute MI. Simultaneously, coronary arteriography emerged as a standard diagnostic tool. Significant advances in the treatment of CAD followed, with the advent of open heart bypass surgery, percutaneous coronary balloon angioplasty, and the insertion of stents. Thereafter, a multitude of large scale randomized, controlled studies demonstrated survival benefits of pharmacologic agents, including beta blockers, platelet inhibitors, angiotensin-converting-enzyme inhibitors, and HMG-CoA reductase inhibitors (statins). Implantable defibrillators, cardiac resynchronization therapy with pacemakers, and left ventricular assist devices have additionally improved survival in patents with heart failure as a result of CAD.
The past two centuries have been host to remarkable and accelerating advances in the diagnosis and treatment of ischemic heart disease. Recent exciting discoveries in genetics, cell-based therapies, and molecular targeting hold promise for the next chapter in the tale for advancing the field of cardiovascular medicine.
Reference: Nabel EG, Braunwald E. A tale of coronary artery disease and myocardial infarction. N Engl J Med 2012;366:54-63