Archive for the ‘Atherosclerotic Heart Disease’ Category
Which Comes First the Chicken or the Egg?
Recently a study was published in the Journal of Sexual Medicine regarding the association of depression, erectile dysfunction and cardiovascular events. J Sex Med 2010; 10.1111/j.1743-6109.2010
Erectile dysfunction has become another issue in patients with cardiovascular disease and risk factors and is fairly common in our society. It is estimated that one in ten males suffer from it. Its definition is the inability to develop or maintain an erection for satisfactory sexual performance. This, of course, is subjective and varies from patient to patient. It is also subjective from couple to couple; and I have had many discussions in my office with couples who are for or against the prescription of drug therapy for this problem.
Erectile dysfunction has been identified and treated as early as the 6th century, and in the past, required various devices or surgical procedures. In 1983, a British physiologist injected himself with phentolamine producing the vasodilatation necessary for erection which heralded a shift in therapy to drugs. And then Viagra came along.
Sildenafil was synthesized in England and patented in 1996. It is an inhibitor of cGMP specific phosphodiesterase type 5 and is responsible for vasodilatation of blood vessels. It was thought to have potential as a treatment for hypertension and angina and was first tested on angina. In Phase I trials for angina, it was found to have no effect on angina but a profound effect on producing erections. The rest, as they say, is history. Viagra was released to market in 1998 and annual sales exceed one billion dollars a year.
Erectile dysfunction is often found in individuals who have hypertension, smoke and have high cholesterol. This also may be an early warning marker of advanced atherosclerosis. It may become another “risk” factor for coronary disease.
The article relates that patients who have erectile dysfunction and are depressed, those with the most depression have the most cardiovascular events; and that depression is an independent factor in their problem. The authors point is that if you are depressed, we as physicians need to find out if you have erectile dysfunction. And if you do, a higher degree of suspicion is warranted for the evaluation of cardiovascular disease. The emphasis on treatment should also be greater and directed against the depression as well as the erectile dysfunction.
Does the depression give you erectile dysfunction or does erectile dysfunction give you depression? Either way this probably goes beyond a locker room joke — although we may as men be fixated on these issues. The issues may well be an early warning sign of deeper problems. If your partner has erectile dysfunction, it may be time to remove it from the bedroom and place it in the doctor’s office.
Share Our Mission to Heal
Holy Cross Hospital is seeking studio audience members for A Mission to Heal, a new show all about the heart.
Needed: 75 audience members for each show; Mix of demographics. No children under 18; Community groups are encouraged to have representation in the audience, as well as community leaders.
Where
A studio in Davie, FL. Details will be provided to audience members upon selection.
When
September 30, 2010; Refreshments will be served.
The show is not “live” but it is being recorded “live” so it will be edited and shown at a later date. Audience members should dress comfortably for long periods of sitting. No white blouses, shirts, hats or sweaters.
Please email info@holy-cross.com and put A Mission to Heal in the subject field OR call 954-776-3244 if you are interested in being part of the studio audience.
Please provide your full name, phone number, e-mail address, age range (20s, 30s, 40s, 50+) and race/ethnicity. Someone will be in touch to let you know if you have been selected and provide additional information.
Vote for the Blog of the Year
Did Dr. Niederman post a blog in 2009 that you found particularly helpful? Was there a blog that you could not wait to share with someone else? We’d love to receive your feedback.
Please comment on what you think was Dr. Niederman’s best blog in 2009.
The Genesis of Implantable Cardiac Defibrillators
The vast majority of people who die from sudden cardiac death are not being monitored in a coronary care unit. Two individuals in particular are responsible for saving the lives of millions of people. One in particular has a truly inspiring story.
Michel Mirowski was born Mordechai Frydman in Warsaw, Poland, in 1924. This was not the time or place to be born Jewish. His father changed his name to Mieczyskaw Mirowski and he blended into the Polish population. He escaped with other Poles to the Ukraine and fought alongside them in the Polish Army. After the war, he returned to Poland, but his family had all been murdered and all his possessions lost. He, like many others, was displaced and he was able to go to Israel. He wanted to become a doctor and as there was no training in Israel, he went to Lyon, France, and entered medical school. He knew neither French nor English but learned both. He was taught in French and studied medical books in English. He married a French women and she called him Michel.
He then studied cardiology in Mexico City, teaching himself Spanish and then went on to Johns Hopkins, where he studied with the great Helen Taussig. When he completed this journey, he went back to Tel Aviv and was the only cardiologist in the hospital. He had a great mentor and teacher in another physician in the hospital. About five years after Mirowski returned, this individual became ill with ventricular tachycardia. Although he was urged to remain in the hospital under observation, he elected to go home and two weeks later he died suddenly during dinner with his family.
Heartbroken, Mirowski began to conceptualize a device that would be implanted in a person to monitor and treat these fatal rhythms. As with most new ideas, everyone said it couldn’t be done. He soon realized that it was not possible to do in Israel and again arrived back in America at Sinai Hospital in Baltimore, Maryland. Here he met Dr. Morton Mower who was the head of the cardiac care unit. Along with Alois Langer, an expert in electrocardiographic signal analysis, these three men went on to develop a device that could be implanted in a patient which would monitor the heartbeat continuously and, if needed, provide life-saving therapy.
Next…why this is so important.
At low risk for cardiovascular events? Aspirin still recommended
Aspirin has long held a place in the secondary prevention of heart attack and death. In other words, there is no controversy about aspirin’s use if you have the diagnosis of atherosclerotic disease. In fact, this is a Class 1A (the highest level) indication in Cardiovascular Guidelines for practice.The controversy is: can we prevent heart attacks and death in patients who have no knowledge of their atherosclerotic burden. This is not a small group of people. It is estimated that 50 million Americans use low dose aspirin regularly for cardioprophylaxis.
Multiple trials have been done with the seminal trial being the Physicians Health Study that started in the mid 1980’s. Basically 22,071 male physicians who were age 40-84 were enrolled. The first problem was they were all men so no knowledge of women’s benefit was gained. They were randomized to take 325mg of aspirin every other day or placebo. Since even physicians are limited, they took the pills from a blister pack and in the aspirin group every other pill was a placebo.
The trial was stopped early because if you were over 50 years of age and a male you had a 44% reduction in heart attacks. A small group had chronic stable angina (i.e. secondary prevention). Although they were “enrolled improperly” the risk reduction of heart attack was 87%. Reduction of stroke and cardiovascular death were found to be inconclusive because of very low rates of occurrence.
Women got their chance in the Women’s Health Study a 40,000 patient trial that showed low dose aspirin did not lower the risk of MI but did lower the risk of stroke.
In 1994 the Antiplatelet Trialist Group published their overview of 174 randomized trials of antiplatet agents. This study included 70,000 high risk patients and 30,000 low risk patients. Again the number of females was unknown. The findings were that long-term antiplatet therapy in patients at high risk of vascular disease offers significant protection against MI, stroke and death. Cardiovascular Guidelines state that among patients with a 10-year cardiovascular risk greater than or equal to 10% this therapy is warranted. See 09/04/09 blog regarding calculating your risk.
Low dose aspirin is used. This is defined as 75-325mg a day. The use of enteric coated does not appear to reduce the risk of GI bleeding complications contrary to common belief. The lower the dose of aspirin used the lower the risk of GI bleeding.
Confused yet? Most doctors are. The best summary is that if patients who are at low risk for cardiovascular events take aspirin for an average of 6.4 years three cardiovascular events are prevented per 1000 women and four cardiovascular events are prevented for men. 2.5 major bleeding events per 1000 occurred among woman and 3.0 per 1000 men.
All About Aspirin
In previous blog posts (08/10/09, 08/16/09) I have reviewed the concept of antiplatelet drugs and their primary role in the protection of patients with coronary atherosclerotic heart disease from heart attack and death. They also serve to help prevent stent closure by clotting. In my next several blogs I will show how, although these concepts seem simple, they continue to engender controversy.
The first controversy again concerns aspirin. I find aspirin’s history compelling. This compound has been in use since ancient times. The active compound acetylsalicylic acid was first prepared by the French chemist Charles Gerhardt in 1853. The name was patented in 1899 after scientists at Bayer decided it was less irritating than salicylate alone. Aspirin soon became quite a hit and now an estimated 40,000 metric tons are used a year.
Two fun facts about aspirin: why is the dose of aspirin 325 mg? It’s because that was the amount of medicine in the tablet that withstood the manufacturing process including the stamping of the Bayer “cross” on the pill. Second, Germany was forced to give up the patent on aspirin in France, Russia, England and the United States after WW I as part of the war reparations.
You would think that since this substance has been around since Hippocrates that we would know how it worked. That piece of science waited until1971 when John Robert Vane showed that aspirin suppressed prostaglandin and thromboxane production. In 1982, he won the Nobel Prize in Medicine for this discovery and was knighted.
Aspirin has been further characterized as a COX-1 (cyclooxygenase enzyme) inhibitor which irreversibly blocks the formation of thromboxane A2 in platelets leading them to lose their ability to form clots. It is this action that we as cardiologists depend upon. The amount of aspirin to accomplish this is small — roughly 40mg a day, which is where the use of 81mg of aspirin gets its recommendation. This is a source of controversy among physicians and in many cases, more aspirin is needed to accomplish the clinical goal of preventing heart attacks, death from cardiovascular causes or stent closure. The more aspirin you take, the higher the likelihood of GI bleed; so that balance is what comes into play.
Next…the beginning of the trials.
Determining Your Risk Level for Developing Heart Disease
Primum non nocere…first do no harm.
The concept as it applies to medicine was first introduced by Hippocrates in his oath of medicine. He wrote “to abstain from doing harm.” Physicians take this oath when we graduate medical school. In modern times it is attributed in the Latin to Thomas Inman in 1860. In general, physicians attempt to apply treatment and procedures that have an overall beneficial effect on patients.
The diagnosis of atherosclerotic heart disease can be quite difficult in patients. Sometimes patients have and express relatively classic signs of exertion angina such as chest pressure that waxes and wanes, sometimes peculiar shortness of breath. Other times it is very difficult to place the symptoms in context.
The Framingham risk score is a system that was developed from the Framingham study (which will be several blogs in the future). Assembling the data allows us to determine the 10-year risk of someone developing symptomatic coronary disease. Those of you who read my blog know our goal as physicians is to reduce the symptoms of coronary disease as we treat the underlying condition with aspirin, statins and medication to control the blood pressure and heart rate.
The score consists of seven questions:
• Age
• Gender
• Total Cholesterol
• HDL Cholesterol
• Smoker
• Systolic Blood Pressure
• Currently on medication for high blood pressure
The higher your Framingham risk scores the higher the risk. You can go online to do it yourself at hp2010.nhlbihin.net/atpiii/calculator.asp
It is those patients who have no symptoms and high risk (> 20%) that demand other techniques to determine the status of their atherosclerotic burden; those in the middle present the largest quandary.
Those techniques are the question, and in my next blog I will discuss the risk of identifying those with coronary disease.
Fish Oil Facts
In my last blog I highlighted the benefit of omega-3 poly unsaturated fatty acids. In the United States there is one FDA approved compound known as Lovaza. This trade name was changed from Omacor because of a name similarity. Fish oil is a combination of two types of fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). In Lovaza this occurs in a fixed amount EPA 465mg and DHA 375 mg. It is recommended to take 500 mg a day if you have no evidence of CV disease and between 800-1,000 mg a day if you do. Those fish oil pills that are brought outside of FDA control have various amounts of these two components and the amounts are represented in different ways, sometimes as a percentage and sometimes as a true amount.
Lovaza was approved for use in patients who have high triglycerides in spite of taking statins. In particular those that have triglycerides over 500 mg/dl. There was a reduction of close to 45% in the active group over the control group.
This whole concept derives from the Mediterranean diet. This is a diet that is advocated by the American Heart Association and consists of eating a diet high in “oily fish” such as salmon, tuna, mackerel and sardines. This is coupled with vegetables particularly tomatoes for improvement in health. Eating these fish twice a week will provide about 500 mg of the compounds and eating it 4-5 times a week yields about 1000 mg of the compounds.
Most find it easier to take the pills than to change their diet but there is no difference between the two approaches. In those patients who are intolerant of statins these compounds provide a useful treatment. I personally do not believe they are a substitute for statins particularly in those patients with documented atherosclerosis.
Talk with your doctor if you want to start them and make sure to look at the bottles to obtain the proper amounts.
Savings Lives One Heart at aTime
Recently, a review article was published in the Journal of the American College of Cardiology. This article reviewed the studies concerning omega-3 polyunsaturated fatty acids, better known as fish oil.
In the United States, physicians generally prescribe statin drugs for the treatment and the prevention of atherosclerotic disease. In Europe it is very common for the treatment protocols to use fish oil pills first and then statins.
The review discussed the varying conditions that were studied. Over 40,000 patients were enrolled in the various trials. These studies involved primary prevention, secondary prevention after sustaining a myocardial infarction heart failure and heart rhythms, such as atrial fibrillation.
Three large trials were done regarding the primary and secondary effects of this compound vs. placebo. Two decades ago the DART (Diet and Reinfarction) showed a 29% reduction in all cause mortality mostly driven by the reduction of cardiovascular mortality. More recently, the GISSI study group randomized over 11,000 patients and found a 15% reduction in the primary endpoint including 21% and 30% reductions in total and CV mortality. This was driven by a 45% reduction in sudden cardiac death.
Additionally, heart rhythms were found to be suppressed by these compounds. These include atrial fibrillation and rhythms which cause sudden cardiac death. Up to a 30% reduction over 12 years was found for atrial fibrillation. We were to participate in a new large trial regarding these compounds which the sponsor cancelled just before inception.
Heart failure is also improved. In a study of patients vigorously treated for heart failure those that took these compounds had an 8-9% reduction in death.
In my next blog I will discuss the various factors you need to know to take these compounds.
The Benefits of Statins
Statins, which if you haven’t guessed by now are one of my favorite topics and are making news again! Two new recently published studies continue to show the tremendous value of these drugs both before you develop the disease of atherosclerosis and after it’s treatment.
A meta-analysis is a process were multiple studies are analyzed together to increase the ability to define value to drugs or medical process. This process has some statistical problems as studies are often enrolled in different ways but in general the technique is regarded as useful to inform us as physicians how to best treat our patients.
Dr Jasper Brugts recently published such a study in the British Medical Journal BMJ 2009; 338:b2376. Titled “The benefits of statins in people without established cardiovascular disease but with cardiovascular risk factors” the analysis showed that statins cut deaths by 12%, coronary events by 30% and cardiovascular events by 19%.
This study looked at ten trials including the recently blogged Jupiter trial ( June 15, 2009). A total of 70,388 subjects without cardiovascular disease but with risk factors for its development were included in this analysis. This effect was seen regardless of age, gender, or diabetic status. It is also important to realize that this effect is in addition to diet and exercise and represents “real world” use.
It is important to discuss with your physicians the use of statins in your case. Targets are LDL < 100. If you already have coronary artery disease the target LDL is < 70. These targets are easily obtained in most cases with today’s drugs. It is not the amount of drug you take it is the drugs measured effect on you. In general, taking more of the drug tends to lead to greater clinical benefit. There is an extremely wide variability to these drugs so comparing your dose to your friend’s dose is of no value. Also, these drugs are everyday drugs and taking them every other day is not advised.
Next…using statins before angioplasty.
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