Evaluation and Management of the Premenopausal Woman with Low BMD

Posted on by MaryO

Current Osteoporosis Reports, 10/31/2013  Review Article  Clinical Article

bone density machine

bone density machine (Photo credit: x1987x)

Cohen A et al. – Interpretation of bone mineral density (BMD) results in premenopausal women is particularly challenging, since the relationship between BMD and fracture risk is not the same as for postmenopausal women. Assessment of markers of bone turnover and follow–up bone density measurements can help to identify those with an ongoing process of bone loss that may indicate a higher risk for fracture, and possible need for pharmacologic intervention.

  • In most cases, Z scores rather than T scores should be used to define “low BMD” in premenopausal women.
  • The finding of low BMD in a premenopausal woman should prompt thorough evaluation for secondary causes of bone loss.
  • If a secondary cause is found, management should focus on treatment of this condition.
  • In a few cases where the secondary cause cannot be eliminated, treatment with a bone active agent to prevent bone loss should be considered.
  • In women with no fractures and no known secondary cause, low BMD is associated with microarchitectural defects similar to young women with fractures; however, no longitudinal data are available to allow use of BMD to predict fracture risk.
  • BMD is likely to be stable in these women with isolated low BMD, and pharmacologic therapy is rarely necessary.

From MDLinx

Menopausal Hormone Therapy

Posted on by MaryO

PS-main-logo

Menopausal Hormone Therapy and Health Outcomes During the Intervention and Extended Poststopping Phases of the Women’s Health Initiative Randomized Trials

JAMA, 10/02/2013  Evidence Based Medicine  Clinical Article

Manson JE et al. – Menopausal hormone therapy continues in clinical use but questions remain regarding its risks and benefits for chronic disease prevention. To report a comprehensive, integrated overview of findings from the 2 Women’s Health Initiative (WHI) hormone therapy trials with extended postintervention follow–up. Menopausal hormone therapy has a complex pattern of risks and benefits. Findings from the intervention and extended postintervention follow–up of the 2 WHI hormone therapy trials do not support use of this therapy for chronic disease prevention, although it is appropriate for symptom management in some women.

Methods

  • A total of 27 347 postmenopausal women aged 50 to 79 years were enrolled at 40 US centers.
  • Women with an intact uterus received conjugated equine estrogens (CEE; 0.625 mg/d) plus medroxyprogesterone acetate (MPA; 2.5 mg/d) (n = 8506) or placebo (n = 8102).
  • Women with prior hysterectomy received CEE alone (0.625 mg/d) (n = 5310) or placebo (n = 5429).
  • The intervention lasted a median of 5.6 years in CEE plus MPA trial and 7.2 years in CEE alone trial with 13 years of cumulative follow–up until September 30, 2010.
  • Primary efficacy and safety outcomes were coronary heart disease (CHD) and invasive breast cancer, respectively.
  • A global index also included stroke, pulmonary embolism, colorectal cancer, endometrial cancer, hip fracture, and death.

Results

  • During the CEE plus MPA intervention phase, the numbers of CHD cases were 196 for CEE plus MPA vs 159 for placebo (hazard ratio [HR], 1.18; 95% CI, 0.95–1.45) and 206 vs 155, respectively, for invasive breast cancer (HR, 1.24; 95% CI, 1.01–1.53).
  • Other risks included increased stroke, pulmonary embolism, dementia (in women aged >=65 years), gallbladder disease, and urinary incontinence; benefits included decreased hip fractures, diabetes, and vasomotor symptoms.
  • Most risks and benefits dissipated postintervention, although some elevation in breast cancer risk persisted during cumulative follow–up (434 cases for CEE plus MPA vs 323 for placebo; HR, 1.28 [95% CI, 1.11–1.48]).
  • The risks and benefits were more balanced during the CEE alone intervention with 204 CHD cases for CEE alone vs 222 cases for placebo (HR, 0.94; 95% CI, 0.78–1.14) and 104 vs 135, respectively, for invasive breast cancer (HR, 0.79; 95% CI, 0.61–1.02); cumulatively, there were 168 vs 216, respectively, cases of breast cancer diagnosed (HR, 0.79; 95% CI, 0.65–0.97).
  • Results for other outcomes were similar to CEE plus MPA.
  • Neither regimen affected all–cause mortality.
  • For CEE alone, younger women (aged 50–59 years) had more favorable results for all–cause mortality, myocardial infarction, and the global index (nominal P < .05 for trend by age).
  • Absolute risks of adverse events (measured by the global index) per 10 000 women annually taking CEE plus MPA ranged from 12 excess cases for ages of 50–59 years to 38 for ages of 70–79 years; for women taking CEE alone, from 19 fewer cases for ages of 50–59 years to 51 excess cases for ages of 70–79 years.
  • Quality–of–life outcomes had mixed results in both trials.

From http://www.mdlinx.com/internal-medicine/newsl-article.cfm/4870253/ZZ4747461521296427210947/?news_id=466&newsdt=100213&utm_source=Newsletter&utm_medium=DailyNL&utm_content=General-Article&utm_campaign=Article-Section

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A Good Night’s Sleep Increases the Cardiovascular Benefits of a Healthy Lifestyle

Posted on by MaryO
sleep

sleep (Photo credit: Sean MacEntee)

A good night’s sleep can increase the benefit of exercise, healthy diet, moderate alcohol consumption and non-smoking in their protection against cardiovascular disease (CVD), according to results of a large population follow-up study.(1) Results showed that the combination of the four traditional healthy lifestyle habits was associated with a 57% lower risk of cardiovascular disease (fatal and non-fatal) and a 67% lower risk of fatal events.(2) But, when “sufficient sleep” (defined as seven or more hours a night) was added to the other four lifestyle factors, the overall protective benefit was even further increased — and resulted in a 65% lower risk of composite CVD and a 83% lower risk of fatal events.

“If all participants adhered to all five healthy lifestyle factors, 36% of composite CVD and 57% of fatal CVD could theoretically be prevented or postponed,” the authors report. “The public health impact of sufficient sleep duration, in addition to the traditional healthy lifestyle factors, could be substantial.”

The study is published today in the European Journal of Preventive Cardiology, and is the first to investigate whether the addition of sleep duration to the four traditional healthy lifestyle factors contributes to an association with CVD.

The Monitoring Project on Risk Factors for Chronic Diseases (MORGEN) is a prospective cohort study in the Netherlands from which 6672 men and 7967 women aged 20-65 years and free of CVD at baseline were followed up for a mean time of 12 years. Details of physical activity, diet, alcohol consumption, smoking and sleep duration were recorded between 1993 and 1997, and the subjects followed-up through a cross-link to national hospital and mortality registers.

As expected, results showed that adherence to each of the four traditional lifestyle factors alone reduced the risk of CVD. Those at baseline who recorded sufficient physical activity, a healthy diet and moderate alcohol consumption reduced their risk of composite CVD from 12% for a healthy diet to 43% for not smoking; and risk reduction in fatal CVD ranged from 26% for being physically active to 43% for not smoking.

However, sufficient sleep duration alone also reduced the risk of composite CVD by about 22% (HR 0.78) and of fatal CVD by about 43% (HR 0.57) when compared with those having insufficient sleep. Thus, non-smoking and sufficient sleep duration were both strongly and similarly inversely associated with fatal CVD.

These benefits were even greater when all five lifestyle factors were observed, resulting in a in a 65% lower risk of composite CVD and an 83% lower risk of fatal CVD.

As background to the study, the investigators note that poor sleep duration has been proposed as an independent risk factor for CVD in two other (non-European) studies, but without adding the effect of sleep to other healthy lifestyle benefits. This study — in a large population — now suggests that sufficient sleep and adherence to all four traditional healthy lifestyle factors are associated with a lower CVD risk. When sufficient sleep duration is added to the traditional lifestyle factors, the risk of CVD is even further reduced.

As an explanation for the results, the investigators note that short sleep duration has been associated with a higher incidence of overweight, obesity and hypertension and with higher levels of blood pressure, total cholesterol, haemoglobin A, and triglycerides, effects which are “consistent with the hypothesis that short sleep duration is directly associated with CVD risk.”

The study’s principal investigator, Dr Monique Verschuren from the National Institute for Public Health and the Environment in the Netherlands, said that the importance of sufficient sleep “should now be mentioned as an additional way to reduce the risk of cardiovascular disease.” “It is always important to confirm results,” she added, “but the evidence is certainly growing that sleep should be added to our list of CVD risk factors.”

Dr Verschuren noted that seven hours is the average sleeping time that “is likely to be sufficient for most people.” An earlier study from her group in the Netherlands, which included information on sleep quality, found that those who slept less than seven hours and got up each morning not fully rested had a 63% higher risk of CVD than those sleeping sufficiently — although those who woke rested, even from less than seven hours’ sleep, did not have the increased risk.(3)

Story Source:

The above story is reprinted from materials provided byEuropean Society of Cardiology (ESC).

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

  1. Hoevenaar-Blom M, Spijkerman AMW, Kromhout D, Verschuren WMM. Sufficient sleep duration contributes to lower cardiovascular disease risk in addition to four traditional lifestyle factors: the MORGEN study. Eur J Prevent Cardiol, 2013 DOI: 10.1177/2047487313493057
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As of Today…

Posted on by MaryO

Cardiac rehab is finished!

WOOHOO

 

The heart attack was January 27, 2013 and it took until today to finish the rehab but it got done.  We’ve both learned quite a bit and I doubt that we’ll ever go back to our earlier way of eating.

What a journey this has been – and I hope it’s done now.

I know that there’s always something else right around the corner but I hope it doesn’t hit us too soon.

Prevent heart attack and stroke

Posted on by MaryO
Generic regular strength enteric coated 325mg ...

Generic regular strength enteric coated 325mg aspirin tablets. The orange tablets are imprinted in black with “L429”. (Photo credit: Wikipedia)

This brief article will provide information and links to where additional information can be found to help you recognize and hopefully prevent a heart attack or stroke.

According to cardiologists, most heart attacks occur in the day, generally between 6 a.m. and noon. If you take an aspirin or a baby aspirin once a day, take it at night. Aspirin has a 24-hour “half-life” therefore, the aspirin would be strongest in your system when most heart attacks happen, in the wee hours of the morning.

A 2012 RetiredBrains survey of cardiologists provides the following information on the symptoms, warning signs and treatment for heart attack and stroke.

How to recognize heart attack symptoms

Chest discomfort that feels like pressure, or seems like a squeezing pain in the center of your chest. This pain generally lasts for more than a few minutes, but sometimes goes away and returns.

Pain and/or discomfort that extends beyond your chest to other parts of your upper body, such as one or both arms, back, neck, stomach, teeth, and even your jaw; shortness of breath, with or without chest discomfort. Other symptoms include: cold sweats, nausea or vomiting, lightheadedness, indigestion, and fatigue.

What should I do when heart attack symptoms occur

If you or someone you are with experiences chest discomfort or other heart attack symptoms the first thing you should do is call 9-1-1.

Don’t wait to make the call. Don’t drive yourself to the hospital. Don’t drive the person having a heart attack to the hospital. Immediate treatment lessens heart damage and can save your life. Emergency medical services personnel can begin treatment in the ambulance on the way to the hospital and are trained to revive a person if his/her heart stops. Some people delay treatment because they are not sure they are really having a heart attack. Remember call 911 immediately as treatment given within an hour of the first heart attack symptoms saves lives and damage to the heart and substantially increases the chances of survival.

What should I do before paramedics arrive

If 911 has been called:

1. Try to keep the person calm, and have them sit or lie down.

2. If the person isn’t allergic to aspirin, have them chew and swallow an aspirin (It works faster when chewed than swallowed whole.)

3. If the person stops breathing, you or someone else who is qualified should perform CPR immediately. If you don’t know CPR, the 9-1-1 operator can assist you until the EMS personnel arrive.

For more information, check out the heart disease section on Mayo Clinic’s site and the warning signs of heart attack, stroke and cardiac arrest, compiled by the American Heart Association.

The information contained in this article should not be substituted for the advice of your physician. If you experience any symptoms or are concerned about your health in any way, you should immediately seek the advice of your physician.

From MarketWatch

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The Difference Between Sudden Cardiac Arrest and Heart Attacks

Posted on by MaryO
Cardiac Arrest Survival

Cardiac Arrest Survival (Photo credit: GEEKSTATS)

, director of cardiology at Johns Hopkins Hospital, talks about the difference between sudden cardiac arrest and a heart attack and what those at risk can do.

Question: What is sudden cardiac arrest?

Answer: Sudden cardiac arrest refers to collapse and loss of consciousness due to a dramatic fall in blood pressure. This is often but not always the result of a life-threatening arrhythmia or an abnormality of the normal rhythmic activity of the heart. An excessively fast or slow heart rate can cause a profound drop in the blood pressure and sudden cardiac arrest. [It] is not a heart attack or myocardial infarction, which refers to a critical blockage in a blood vessel that supplies blood, oxygen and nutrients to the heart muscle. A blockage in a blood vessel can cause part of the heart muscle to die and be replaced by scar.

Q: How common is it, and who is at risk?

A: The risk factors for sudden cardiac arrest include the presence of heart disease, a family history and many of the factors that increase the risk for a heart attack, such as smoking, obesity, physical inactivity, high blood pressure, high cholesterol, high blood sugar or diabetes, and a poor diet. If someone has heart disease, particularly with weakness of the heart muscle, they may be at particularly high risk for sudden cardiac arrest and may benefit from implantation of an Implantable Cardioverter Defibrillator. [The defibrillators] may also benefit patients with a family history of sudden cardiac arrest and/or a genetic tendency to arrhythmias.

Q: How can you prevent sudden cardiac arrest?

A: In some cases, sudden cardiac arrest can be brought on by exertion, but this is not always the case, as sudden cardiac arrest often occurs when one is at rest. Physical activity is generally good for all of us. Those with known heart disease should consult their health care provider about the details of their own physical activity, but generally, even patients with heart disease should try to remain active. It’s wise to avoid extreme activity, particularly in harsh environmental conditions, such as heat or cold. For anyone who exercises, symptoms such as profound dizziness or lightheadedness, chest pain, shortness of breath, extreme fatigue and/or palpitations should prompt cessation of exercise and depending upon the severity of the symptoms and get prompt medical attention.

Q: How is sudden cardiac arrest different from a heart attack?

A: Heart attacks are caused by blockage of the arteries, which supply oxygen and nutrients. These most often are accompanied by chest pain and/or shortness of breath. Sudden cardiac arrest can be a complication of a heart attack, but it can occur without a heart attack. The treatment of a heart attack is to limit the damage to the heart by promptly opening up the involved blood vessel by a procedure known as angioplasty and by placing a stent to keep that vessel open. The treatment of sudden cardiac arrest is restoration of the heart’s normal rate of contraction and rhythm, and this typically involves a shock to the chest that’s known as cardioversion or defibrillation.

Q: How quickly do you need to be treated to survive?

A: The most common arrhythmias or irregularities of the heart that cause sudden cardiac arrest are rapid heart rhythms from the heart’s lower chamber. These are called ventricular tachycardia and ventricular fibrillation. If these arrhythmias are not promptly corrected by a shock to the chest, the individual will die. In the case of ventricular fibrillation, this may take only minutes. One can buy time by performing effective CPR. Just chest compressions, or so-called “hands-only” CPR, can be lifesaving.

Adapted from The Baltimore Sun

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Blood Pressure Infographic

Posted on by MaryO

A Snapshot: Blood Pressure in the U.S. Make Control Your Goal. High blood pressure is a major risk factor for heart disease and stroke, the first and fourth leading causes of death for all Americans. High Blood Pressure Basics. 67 million American adults—1 in 3—have high blood pressure. High blood pressure contributes to ~1,000 deaths/day. When your blood pressure is high, you are 4 times more likely to die from a stroke, and you are 3 times more likely to die from heart disease. 69% of people who have a first heart attack, 77% of people who have a first stroke, and 74% of people with chronic heart failure have high blood pressure. Annual estimated costs associated with high blood pressure: $51 billion, including $47.5 billion in direct medical expenses. Blood Pressure Control. Only about half of people with high blood pressure have their condition under control. Reducing average population systolic blood pressure by only 12–13 mmHg could reduce stroke by 37%, coronary heart disease by 21%, deaths from cardiovascular disease by 25%, and deaths from all causes by 13%. Make Control Your Goal, Every Day. Check your blood pressure regularly—at home, at a doctor’s office, or at a pharmacy. Eat a healthy diet with more fruits, vegetables, potassium, and whole grains and less sodium, saturated fat, trans fat, and cholesterol . Read nutrition labels and lower your sodium intake. Most of the sodium we eat comes from processed and restaurant foods. About 90% of Americans eat too much sodium. Quit smoking—or don’t start. 1-800-QUIT-NOW or Smokefree.gov. Adults should limit alcohol to no more than 1 drink per day for women and 2 drinks per day for men. Get active and maintain a healthy weight. Aim for 2 hours and 30 minutes of moderate physical activity every week. This infographic was developed by the Centers for Disease Control and Prevention’s Division for Heart Disease and Stroke Prevention in support of achieving the Million Hearts® initiative goal to prevent 1 million heart attacks and strokes by 2017.

Test your blood pressure IQ using our new infographic! How many facts about blood pressure did you already know?

Food…

Posted on by MaryO

…in a nutshell <ahem!>

good-food-bad-food

Hypercortisolism Is Associated With Increased Coronary Arterial Atherosclerosis

Posted on by MaryO

Hypercortisolism Is Associated With Increased Coronary Arterial Atherosclerosis: Analysis of Noninvasive Coronary Angiography Using Multidetector Computerized Tomography

Journal of Clinical Endocrinology and Metabolism, 05/21/2013  Clinical Article

  1. Nicola M. Neary*,
  2. O. Julian Booker*,
  3. Brent S. Abel,
  4. Jatin R. Matta,
  5. Nancy Muldoon,
  6. Ninet Sinaii,
  7. Roderic I. Pettigrew,
  8. Lynnette K. Nieman and
  9. Ahmed M. Gharib

–Author Affiliations


  1. Program in Reproductive and Adult Endocrinology (N.M.N., L.K.N., B.S.A.), Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892; Laboratory of Cardiac Energetics (O.J.B.), National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892; Integrative Cardiovascular Imaging Laboratory (J.R.M., R.I.P., A.M.G.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Critical Care Medicine (N.M.), Clinical Center, National Institutes of Health, Bethesda, Maryland 20892; and Biostatistics and Clinical Epidemiology Service (N.S.), Clinical Center, National Institutes of Health, Bethesda, Maryland 20892
  1. Address all correspondence and requests for reprints to: Ahmed M. Gharib, MB, ChB, National Institutes of Health, Building 10, Room 3-5340, Mail Stop Code 1263, 10 Center Drive, Bethesda, MD 20892. E-mail: agharib@mail.nih.gov.

  1. ↵* N.M.N. and O.J.B. contributed equally to this work.

Abstract

Background: Observational studies show that glucocorticoid therapy and the endogenous hypercortisolism of Cushing’s syndrome (CS) are associated with increased rates of cardiovascular morbidity and mortality. However, the causes of these findings remain largely unknown.

Objective: To determine whether CS patients have increased coronary atherosclerosis.

Design: A prospective case-control study was performed.

Setting: Subjects were evaulated in a clinical research center.

Subjects: Fifteen consecutive patients with ACTH-dependent CS, 14 due to an ectopic source and 1 due to pituitary Cushing’s disease were recruited. Eleven patients were studied when hypercortisolemic; 4 patients were eucortisolemic due to medication (3) or cyclic hypercortisolism (1). Fifteen control subjects with at least one risk factor for cardiac disease were matched 1:1 for age, sex, and body mass index.

Primary outcome variables: Agatston score a measure of calcified plaque and non-calcified coronary plaque volume were quantified using a multidetector CT (MDCT) coronary angiogram scan. Additional variables included fasting lipids, blood pressure, history of hypertension or diabetes, and 24-hour urine free cortisol excretion.

Results: CS patients had significantly greater noncalcified plaque volume and Agatston score (noncalcified plaque volume [mm3] median [interquartile ranges]: CS 49.5 [31.4, 102.5], controls 17.9 [2.6, 25.3], P < .001; Agatston score: CS 70.6 [0, 253.1], controls 0 [0, 7.6]; P < .05). CS patients had higher systolic and diastolic blood pressures than controls (systolic: CS 143 mm Hg [135, 173]; controls, 134 [123, 136], P < .02; diastolic CS: 86 [80, 99], controls, 76 [72, 84], P < .05).

Conclusions: Increased coronary calcifications and noncalcified coronary plaque volumes are present in patients with active or previous hypercortisolism. Increased atherosclerosis may contribute to the increased rates of cardiovascular morbidity and mortality in patients with glucocorticoid excess.

  • Received October 29, 2012.
  • Accepted March 7, 2013.

From JCEM

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Classifying hypertension

Posted on by MaryO

HYPERTENSION is classified into two categories according to its cause: essential and secondary.

The vast majority of patients have essential or primary hypertension, while only about 5-10% of patients have secondary hypertension, which are mainly caused by kidney and hormonal conditions like renal artery stenosis, hyperthyroidism, Cushing’s syndrome, and even pregnancy, among others.

The exact cause of essential hypertension is still unknown, although it is certainly the result of a combination of factors, including increasing age, having relatives with high blood pressure (ie family history), a sedentary lifestyle, a poor diet with too much salt, drinking too much alcohol, smoking and too much stress.

English: blood pressure measurement Deutsch: :...

English: blood pressure measurement Deutsch: :deBlutdruckmessung (Photo credit: Wikipedia)

Says Malaysian Society of Hypertension president and Universiti Malaya Department of Primary Care Medicine senior consultant Prof Datin Dr Chia Yook Chin: “Each factor increases blood pressure by just a little, but when you add them all together little by little, it raises it by quite a lot.”

Despite not knowing the root cause of hypertension, it has been established that there is overstimulation of the sympathetic nerves in people with this condition.

This in turn increases the secretion of certain hormones involved in the regulation of sodium and fluids in the body, called renin, angiotensin, and aldosterone.

The amount of salt and water in our body affects our blood pressure – the more salt and water present, the higher our blood pressure.

These two elements are regulated by our kidneys through the three hormones mentioned above, which are produced by the adrenal glands located on top of the kidneys.

The overstimulation of the sympathetic nerves also results in increased vascular tone, which causes our arteries to become constricted, thus, also raising blood pressure.

From The Star

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