Heart Attack and Stroke Risk Questions Answered by Cardiologists

Heart Attack and Stroke Risk Questions Answered by Cardiologists

CRP and Family History

Question: I am a 39-year-old woman in relatively good shape and with good eating habits, but I have a history of heart disease in my family. My question concerns C-reactive protein (CRP) results. I had a result of 9.3 mg/L in 2011; a re-test using ultrasensitive CRP of 6.6 mg/L in 2011; and just recently, in 2012, a result of 6.52 mg/L. The results are listed as high according to one of the labs, and the other lab lists them as within the normal range. My cholesterol is 176; my high-density lipoprotein (HDL) is 56, and my low-density lipoprotein (LDL) is 77. I'm not sure what to do next. With a family history of heart disease, what steps should I take?

Answer: Congratulations on maintaining a healthy lifestyle. Your confirmed C-reactive protein (CRP) measurement is indeed high. If these measurements were made on blood that was sampled when you were not ill (sick with a fever, for example), and if you do not have a chronic inflammatory condition such as rheumatoid arthritis, this result indicates that you have an increased risk of cardiovascular disease, according to our best evidence today.

You do not mention the age at which people in your family have had heart disease, or what kind of heart disease they have had. If your mother or father had a heart attack before age 60, that family history further elevates your estimate of cardiovascular risk. You can check your cardiovascular risk using a calculator developed and validated by my colleagues at BWH, Drs. Paul Ridker and Nancy Cook. This tool, known as the Reynolds risk score, takes CRP and family history into account in addition to traditional risk factors.

Even with these indicators of elevated risk, your actual absolute risk of having a heart event is estimated at under 1% over 10 years, due to your youth and female sex, assuming that your blood pressure is normal and that you do not smoke. Over your lifetime, however, your risk is greater than those without heart disease in the family and without high CRP. These considerations should serve as an additional stimulus to maintain your healthy lifestyle.

A large clinical trial known as JUPITER showed that women considerably older than you, but who, like you, have below-average cholesterol but CRP greater than 2 mg/dL, had substantially reduced cardiovascular events when treated with a statin drug. Because of your relative youth, the results of the JUPITER study may not apply to you. I would advise you to talk with your doctor about the pros and cons of statin treatment in your case.

Calcium-scoring Test

Question: I am a 56-year-old woman in good general health. I eat right, exercise moderately, and have never been overweight. My blood pressure is low to normal. Because of a family history of high cholesterol (my levels most recently: low-density lipoprotein [LDL], 150; high-density lipoprotein [HDL], 90; lipoprotein(a) [Lp(a)], 150; C-reactive protein [CRP], 0.02), my family doctor sent me for a calcium-scoring test. The result was 396, with 350 of it in the left anterior descending artery. The radiologist marked this as "moderate," but it didn't sound moderate to me, so I went to a cardiologist — who also gave an assessment of "moderate." He does not normally use this test. Because I have no overt symptoms, he is putting me on niacin (Niaspan) and a statin. What I need is a straight answer: How bad is my situation? Should other tests be done?

Answer: First, congratulations to you and your doctor for not rushing to the cardiac catheterization laboratory in the absence of symptoms, and for starting a sensible preventive regimen. Your story brings up several interesting and important points that I’ll comment on one by one.

You describe a family history of high cholesterol, but your own cholesterol (LDL, 150), though above ideal, is not in the range attributed to the simple genetic abnormalities associated with high cholesterol. In your case, I am more interested in a family history of “premature” cardiovascular events in first-degree relatives — for example, a heart attack that occurred in a parent at less than 60 years of age. Such a family history would elevate your estimated risk for cardiovascular disease more than even a full battery of genetic tests that could be performed today (but are not yet recommended or available in routine practice.)

The next important point regards the Lp(a). While you don’t give units or the normal values of the laboratory that performed this test, by usual standards (mg/dL or milligrams per deciliter), 150 is quite high. Lp(a) (pronounced “L P little a”) is a genetically-influenced risk factor for atherosclerotic events, consisting of a low-density lipoprotein particle (“bad cholesterol”) combined with a protein known as apolipoprotein (a). High levels of Lp(a) can run in families, and cause an increase in events caused by atherosclerosis.

We do not have many therapeutic options to treat high levels of Lp(a), nor do we have large-scale clinical trials that validate the use of treatments to lower the risk associated with high Lp(a). But in medicine we often have to manage problems without definitive proof of efficacy, and with limited tools — the treatment of high Lp(a) falls into this category.

One approach is to lower LDL, a part of the Lp(a) complex, so your doctor starting you on a statin makes perfect sense. Nicotinic acid, or niacin, in doses of several grams a day (usually given as a sustained-release dosage form), can also lower Lp(a), so your doctor’s decision to start you on niacin also has a reasonable basis — although, like statins, this treatment has not been proven to lower cardiovascular events in people with high levels of Lp(a). Some new medicines currently being tested also lower Lp(a), and we may have more tools in this regard in the future.

The next point concerns the CRP, reported as 0.02. You do not give the units, and in the case of CRP, this is very important. If your CRP was measured with a highly sensitive assay (hsCRP), and the result is reported in mg/L (milligrams per liter), it indicates a low level of inflammation — one marker of cardiovascular risk. If the value was reported in milligrams per deciliter, it corresponds to 2 mg/L — a level in the intermediate “yellow light” zone for cardiovascular risk assessment. Either way, I do not think that the CRP would be decisive in the management of your case, given the elevated risk conferred by the high Lp(a) in the context of an above-ideal LDL level.

And then we come to the calcium score. This test in your case suggests that you have atherosclerosis — or hardening of the arteries — and indicates an increase in cardiovascular risk, a point we already know from the above-ideal LDL level and the high Lp(a). So from my clinical vantage point, the calcium score doesn't really add new information to your case.

Too often, doctors reflexively send patients, understandably alarmed by an abnormal calcium score, for invasive testing such as a coronary arteriogram. The problem with this approach is that many fatty plaques that can cause sudden heart attacks may not cause arterial narrowing visible on the angiogram, because they grow outward, without impinging on the artery’s flow channel — so an angiogram that shows no tight blockage does not mean that the individual has no risk of a heart attack.

On the other hand, not all blockages that show up on angiogram need treatment by angioplasty, inserting a stent, or bypass surgery. Our best evidence today shows that a good risk-reduction regimen via lifestyle and medications can yield results that are as good as with invasive revascularization for many patients. That is why I congratulated you and your doctor for not rushing towards an angiogram, but instead instituting non-invasive preventive therapy. In the absence of symptoms, your doctor’s approach seems quite sensible.

You asked whether additional tests should be done, and you state that you engage in moderate exercise. The additional test that I might consider would be a treadmill exercise test, monitoring an electrocardiogram and symptoms to see if with stress, you develop signs of part of the heart not receiving enough blood flow — but which, for one reason or another, is not causing symptoms. This is not a perfect test; electrocardiogram findings in women may be less reliable than in men.

An abnormal electrocardiogram at rest can make a stress study difficult to interpret. Yet, a high exercise capacity without symptoms or signs of impaired blood flow the heart could reassure you and your doctor that you are on the right track with adhering to a good lifestyle and medical therapy program.

A final point revolves around the issue of familial risk. As high levels of Lp(a) can run in families, you should discuss with your doctor screening of any offspring you may have for this risk factor. As I emphasized above, we do not have definitive data that intervening on high Lp(a) can lower risk. Nonetheless, if you have first-degree relatives with a high level of Lp(a), they would be well advised to pay particular attention to lifestyle measures to limit cardiovascular risk, and to receive careful follow-up.

“Soft” Plaques and “Hard” Plaques

Question: I am a 45-year-old Indian man. I have been hypertensive for the last 10 years, but it is well controlled (at 120/70 most of the time) with ramipril (2.5 mg). At a recent visit with my cardiologist, he performed an electrocardiogram (ECG) and observed some changes, from which he advised a computed tomography (CT) angiogram.

The results were as follows:

  • Heart rate during test: 57-60 bpm (beats per minute). Normal sinus rhythm noted.
  • Coronary calcium score (Agastson): 0.
  • Left main coronary artery (LMCA): normal in caliber, no plaques.
  • Left anterior descending artery (LAD): type-III vessel; eccentric soft plaque noted at proximal LAD, causing mild luminal narrowing (30%); mid and distal segments, normal in caliber, no plaques.
  • D1: normal in caliber, no plaques, shows distal branch.
  • D2: normal in caliber, no plaques.
  • D3: Eccentric soft plaque noted at proximal D3, causing mild luminal narrowing. Mid and distal segments are normal in caliber, no plaques.
  • D4: Normal in caliber. No plaques.
  • Left circumflex artery (LCX): Normal in caliber, no plaques.
  • OM1 & OM2: Small caliber vessel. No plaques.
  • OM3: Large caliber vessel. No plaques.
  • Right coronary artery (RCA): Dominant. Normal in caliber. No plaques.
  • PLVB & PDA: supplied by RCA. Early PLV noted arising from distal RCA followed by another
  • PLV 2 branch. PLV and PDA show normal caliber. No plaques.
  • Extracoronaries: Aorta: Moderate atherosclerotic disease noted more so in the left carotid and subclavian arteries.
  • Pulmonary vessels, aortic & mitral valves, left atrium & its appendage, myocardium, pericardium all are normal with no calcification.

My doctor advised me to take enteric-coated aspirin (75 mg) and rosuvastatin (10 mg). I also take ranolazine (extended release, 100 mg). Are all these medications necessary? I am more worried about the eccentric soft plaques noted in the test results, as I have heard that they are more dangerous than hard plaques. Are they very serious? Another cardiologist said I should have a regular angiogram in addition to the CT angiogram. Do you think this is necessary? I would appreciate your assessment and guidance.

Answer: Thank you for your question. You do not specify what findings on the electrocardiogram triggered the computed tomographic angiogram (CTA) that you describe in detail — those findings help me to get a full picture of your situation. The CTA does show a “soft” plaque, and other findings that show that you have some atherosclerosis. That said, let me answer your specific questions individually.

You ask whether “soft” plaques are in fact more dangerous than “hard” plaques. As the CTA does not actually measure softness or hardness, I prefer the terms “low attenuation” versus “calcified” plaque. Some evidence indeed shows that low attenuation plaque can cause heart attacks more frequently than calcified plaques. In practical clinical terms, however, my interpretation of your findings is that you are a good candidate for intensive risk reduction through lifestyle modification and medical therapy.

You inquire whether you should undergo invasive coronary arteriography. Once again, I do not have a full picture, not having access to your electrocardiogram. In the absence of symptoms or signs on a rest or stress electrocardiogram that part of the heart is not receiving enough blood, management with lifestyle and medical preventive therapy would be indicated, and the findings of an invasive angiogram would not alter this recommendation.

You then ask if all of the medications you list are required. You describe a history of high blood pressure that has responded to ramipril. Given this history, your risk profile, and our current knowledge base about ramipril, I would recommend continuing that medication.

The evidence for benefit of low-dose aspirin therapy for people who have not had a heart attack is not nearly as compelling as the evidence for reduction of recurrent cardiovascular events in those who have already had an event. Yet, given your risk profile, if you do not have any bleeding problems, it is not unreasonable to continue the aspirin.

You do not include information regarding your blood cholesterol levels (lipid profile); I therefore cannot comment on the dose of the statin that you are taking. But given what you have included, I would not stop taking the statin.

Regarding the ranolazine, I don't understand why that was recommended from the information you provide. Generally, this medicine is given to help control symptoms of chest pain due to restricted blood flow to the heart muscle (angina pectoris). It also may have some effect on the heart rhythm, but that is not generally an indication for starting the drug.

Given your young age, and the risk factors you describe, I congratulate you on and aggressive stance regarding lifestyle and medications. Incidentally, your question indicates that the results of the CTA are causing you some anxiety. It is not clear to me from the data available that this particular test was necessary to refine your cardiovascular risk assessment. This situation is an example of the limitations of medical technology: an expensive test that involves radiation exposure has caused you considerable concern, without necessarily leading to a change in your management that we know can reduce your risk.

Mast Cell Activation Disorder, Allergies, and Cardiovascular Disease

Question: I have mast cell activation disorder and receive treatment from allergy physicians at Brigham and Women’s Hospital. Are you aware of any cardiovascular diseases that may be accelerated or negatively impacted by this disorder?

Answer: A spate of recent laboratory studies supports the participation of mast cells in atherosclerosis and in arterial aneurysm formation. Most of these studies derived from observations in mice, and using biomarkers of mast cell activation in humans. But direct evidence that mast cells aggravate human cardiovascular disease remains scant.

My best general advice to you is to heed current guidelines regarding cardiovascular prevention assiduously, to minimize any excess risk you might have from an underlying mast cell activation disorder. I'm sure that your Brigham and Women's Hospital physician would be happy to refer you to a member of our preventive cardiology staff, should you need any guidance in this regard.

Cardiovascular Benefits of Meditation

Question: In theorizing about cardiovascular workout benefits, I came up with a question that I couldn't find an answer to on the Web. If a person could raise his or her heart rate through meditation instead of actual muscular movement, would he or she still see any of the health benefits of cardiovascular exercise? And could any negative effects result from blood and nutrients being forced into places in the body that aren't in need of the surplus, because they aren't actually working harder? Before experimenting with this, I wanted to be aware of anything I should watch out for; I also plan to continue my regular cardiovascular exercise routine.

Answer: The cardiovascular benefits of physical activity depend not only on effects on the heart, but also those on skeletal muscle (not to mention weight control.) While increasing heart rate without muscular movement might provide some training effect on the heart muscle, it would not improve the strength or metabolic efficiency of the much greater mass of skeletal muscle.

There are many and marvelous layers of regulation of blood supply to body tissues, such that any increase in the output of the heart due to an increase in heart rate would not necessarily force blood and nutrients to organs that don't need them.

Much observational data support the cardiovascular benefits of regular physical activity. Meditate by all means if it makes you feel better, but currently, more evidence supports the long-term health benefits of regular physical activity. It would be great though to have more rigorous studies of alternative and complementary approaches to cardiovascular risk reduction, to expand our preventive horizons.

Calcium Score

Question: I just received a CAC score of 962. What cardiology office at Brigham and Women’s Hospital should I contact for a follow-up? Is there anything I should do immediately, before seeing a physician?

Answer: Interpreting the results of a calcium score requires a full cardiovascular risk assessment. I cannot give you advice based on a number alone; you should seek a full history, physical examination, and laboratory assessment, and possibly a stress test.

I’m curious as to why you had a heart calcium scan done before seeing a physician, as your question implies. I personally discourage the use of any imaging technique as a way to screen individuals for cardiovascular risk before they've had a clinical evaluation. While calcium scans may indicate disease, we do not have studies that show the benefit of interventions guided by calcium scores.

In contrast, we have a wealth of data that show that we can effectively manage many aspects of cardiovascular risk that we can assess by a simple history, physical examination, and some relatively inexpensive lab tests that don’t involve radiation. In any case, we would be pleased to arrange a visit for you with one of our cardiovascular prevention specialists. Please call 1-800-294-9999.

Imaging Tests to Diagnose Coronary Artery Disease (CAD)

Question: Who is considered a good candidate for the 64-slice CT scan instead of an angiogram to diagnose CAD? Is the amount of radiation exposure from the CT scan dangerous?

Answer: The appropriate use of imaging tests to diagnose coronary artery disease (CAD) depends on the situation. For apparently well people without heart symptoms, I do not favor the use of any imaging test for screening for CAD. Simple risk calculators can be used to estimate an individual’s risk for cardiovascular events.

For individuals with symptoms suggestive of CAD, a stress test monitored by electrocardiogram is often a good place to start. For those without symptoms, but at high risk for CAD based on non-imaging markers such as the scores referenced above, imaging tests may provide useful information for management. You should discuss with your cardiologist about whether you fit into this category.

Computed tomographic angiography of the heart (coronary CTA) is evolving rapidly and may become part of routine practice in those with symptoms, elevated calculated risk, or a positive stress test. Currently, the level of radiation is on the same order as a cardiac catheterization with traditional invasive angiography. Technical advances are rapidly lowering the amount of radiation required for coronary CTA. Even so, such tests should not be used for routine surveillance on a repetitive basis.

Intravascular Ultrasound (IVUS)

Question: Is intravascular ultrasound (IVUS) a standard procedure at Brigham and Women’s Hospital, or is it still experimental? What are the patient circumstances (i.e., clinical presentation) that would trigger the recommendation of an IVUS procedure over angiography? Do most insurance companies pay for this procedure?

Answer: Intravascular ultrasound is an invasive procedure limited to special applications in clinical practice. It is also a research tool that has increased our understanding of coronary atherosclerosis in humans. Its main use is in the invasive cardiology laboratory during cardiac catheterization in special circumstances, to help define coronary artery anatomy in conjunction with an x-ray angiogram.

The invasive specialist may occasionally use intravascular ultrasound to ascertain the optimum deployment of a stent, or to guide interventional management in special cases. Intravascular ultrasound is certainly available at Brigham and Women’s Hospital, but it is never a first-line test for the diagnosis of coronary artery disease.

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