Circulation. 2005;112:297
(Circulation. 2005;112:297.)
© 2005 American Heart Association, Inc.
Issue Highlights
 |
CORTISOL, TESTOSTERONE, AND CORONARY HEART DISEASE: PROSPECTIVE EVIDENCE FROM THE CAERPHILLY STUDY, by Smith et al.
|
|---|
There are abundant animal and human data as well as lay support
for the concept that chronic stress predisposes to heart disease.
However, the pathophysiological basis of the stress-heart disease
connection remains poorly understood. In a prospective observational
study of middle-aged men in Caerphilly, South Wales, Dr Davey
Smith and colleagues examined whether elevated cortisol-to-testosterone
ratio, a reputed biological marker of stress, increased the
risk of ischemic heart disease. The investigators observed that
there was a dose-response relation between increasing levels
of cortisol to testosterone and the longitudinal development
of ischemic heart disease, but no other causes of death. When
the authors further adjusted for components of the insulin resistance
syndrome, the relation with ischemic heart disease was significantly
attenuated. The researchers acknowledged that their findings
will need to be replicated in other study cohorts and with other
designs. However, given that it is unlikely that chronic stress
will be eliminated from modern life, understanding the biology
of the stress-coronary artery disease connection will be important
to facilitate the development of effective stress prevention
and treatment strategies. See p
332.
 |
STATIN THERAPY MAY BE ASSOCIATED WITH LOWER MORTALITY IN PATIENTS WITH DIASTOLIC HEART FAILURE: A PRELIMINARY REPORT, by Fukuta et al.
|
|---|
The pathophysiology and therapy of heart failure with a normal
ejection fraction remain poorly understood. Fukuta et al examined
the relationship between survival and the type of therapy in
137 patients with clinical heart failure and an ejection fraction

0.50. Although the number of deaths was small, there was a strong
relationship between the use of a statin and survival, whereas
no apparent relationship was found for angiotensin-converting
enzyme inhibitors, angiotensin receptor blockers, or ß-blockers.
Serum LDL was higher in the statin-treated patients, as was
the incidence of several other risk factors for heart failure,
including hypertension, diabetes, and coronary artery disease.
The relationship between statin use and survival persisted after
adjustment for baseline clinical variables. If confirmed by
controlled trials, these observations may provide a valuable
new approach to the treatment of heart failure with a normal
ejection fraction. See p
357.
 |
EIGHT-YEAR FOLLOW-UP OF PATIENTS WITH PERMANENT VENA CAVA FILTERS IN THE PREVENTION OF PULMONARY EMBOLISM: THE PREPIC (PRÉVENTION DU RISQUE DEMBOLIE PULMONAIRE PAR INTERRUPTION CAVE) RANDOMIZED STUDY, by The PREPIC Study Group
|
|---|
Approximately 8 years ago, the initial report from the PREPIC
study was published, demonstrating that permanent vena cava
filters reduced the incidence of pulmonary embolism but were
associated with increased deep-venous thrombosis at 2 years.
The long-term effect of vena cava filters remained unknown.
In this issue of
Circulation, the follow-up on the 400 patients
randomized to either receive a filter or be treated with medical
therapy is reported. At 8 years, the investigators report that
the initial observations of reduced pulmonary embolism and increased
deep venous thrombosis remain; however, they now find no effect
on survival. The use of vena cava filters continues to be a
complicated decision, but findings such as these suggest that
there is unlikely to be survival benefit in low-risk patients.
See p
416.
Visit http://www.circ.ahajournals.org:
 |
Cardiology Patient Page
|
|---|
Antiphospholipid Antibodies. See p
e39.
 |
Images in Cardiovascular Medicine
|
|---|
A Nest in the Chest. See p
e45.
Fusion Imaging Between Myocardial Perfusion Single Photon Emission Computed Tomography and Cardiac Computed Tomography. See p e47.
Extensive Subepicardial Fibrosis in a Patient With Apical Hypertrophic Cardiomyopathy With Persistent ST-Segment Elevation Simulating Acute Myocardial Infarction. See p e49.
 |
Correspondence
|
|---|
See p
e51.