Cardiovascular Risk Factors (Dr. Hazen 9/6/11)
Tuesday, September 6, 2011 - Noon
Stanley Hazen MD, PhD
Section Head, Preventive Cardiology & Rehabilitation Department of Cardiovascular Medicine Miller Family Heart & Vascular Institute
Cardiovascular disease is by far the leading cause of death in the United States. Therefore, knowing your risk factors and treating them early is vitally important. Dr. Hazen answers questions about cardiovascular risk factors.
Cleveland_Clinic_Host: Welcome to our "Cardiovascular Risk Factors" online health chat with Stanley Hazen, MD, PhD. He will be answering a variety of questions on the topic. We are very excited to have him here today! Thank you for joining us, let's begin with the questions.
Dr__Stan_Hazen: Thank you for having me.
Secondary Prevention: Stop the Progression of Cardiovascular Disease
Peppy: How can I slow or stop the progression of this awful disease? I had one stent over three years ago. Cardiologist checked the carotids last year and said they are both 50% occluded. I would love to see the carotids and heart arteries stay the same or regress. Is that possible?
Dr__Stan_Hazen: Halting progression, and even promoting regression, is possible. In general, lowering LDL (bad) cholesterol to < 70 halts progression in most individuals, and can even help promote regression. In some, even lower and more aggressive overall preventive goals are needed. If possible, in someone who has progressive disease despite having LDL at goal, we can even aim for far lower goals (actually - there is no LDL that is "too low" as far as we are aware, but most of the major clinical trials have used 25 as the emergency cutoff, below which we do not drive the LDL down).
Bring the LDL to ultra low levels (e.g. 30s-50s) helps to calm down the inflamed artery wall, and often is what we aim for in someone with progressive disease and recurrent events/restenosis despite otherwise being at the national guideline stated goals.
Peppy: Thank you for spending your time answering our questions. I had a stent placed over three years ago, and just found out my carotids are 50% occluded. What can I do to stop this progression or slow/stabilize it? Meds, exercise are a given. Diet is confusing with so much information circulating.
Dr__Stan_Hazen: The same approach for halting progression of coronary artery atherosclerosis also helps to reduce carotid atherosclerosis. Thus, a major effort is to lower the LDL to < 70 (minimum), along with BP control, weight reduction if needed, dietary efforts, monitoring for diabetes or prediabetes, etc. In addition, stroke preventive efforts are key. These include improved BP control (120/80 is the goal), platelet prophylaxis therapy (low dose aspirin as long as there are no contraindications). The carotids should be monitored annually given you have known plaque there (50% stenosis). If they progress to 8% or more, then intervention is likely warranted.
janpersico: What is the current "state of the art" for individualizing a treatment plan for someone with advanced disease, history of MI, 3 cardiac stents, 1 carotid stent?
Dr__Stan_Hazen: The current "state of the art" for someone with known CAD is to go after each and every possible risk reduction aspect of preventive health one can. A global effort to lower lipids, adopt good diet, weight loss if needed, BP control, etc. Most subjects with documented CAD and history of MI and stent end up on a cocktail of meds including a statin, low dose aspirin, beta blocker, ACEI or ARB, and plavix or other anti-platelet medication. Omega 3 FA supplementation also is often considered, especially if TG are in any way elevated.
Primary Prevention Efforts
cohnanita: IF my father died at age 58 a week after MI with pulmonary edema, what about my risk factors for cardiovascular disease. I HAVE ALSO A MECHANICAL MITRAL VALVE AND HEART RHYTM PROBLEMS.
Dr__Stan_Hazen: Having a first degree relative with premature cardiac disease increases your risk. You should have your lipid profile checked, your BP checked, and look for screening tests for diabetes. I also would check an LP(a) level, a risk marker that runs in families and is associated with increased heart attack, stroke and death risk. Having a mechanical valve and rhythm abnormalities in of themselves are not risk factors for atherosclerotic heart disease.
hite01: I have an extremely strong family history of heart disease and early death from my mother's side of the family. I am doing all I can to prevent any heart problems. I am taking 10mg of Zocor to stave off high cholesterol. Last readings were very good. I also have mitral valve prolapse which causes my heart to beat out of rhythm at times. Is there anything I can do to prevent a heart event given my strong family history?
Dr__Stan_Hazen: As noted in a different question - in those with strong family history, one can check the LP(a) level. If it is high (>30), then we recommend more aggressive LDL goals (<70).
Other global cardiac risk reduction approaches should be undertaken beyond simply cholesterol monitoring. This includes BP, weight, diet, blood sugar, and exercise efforts. Low dose aspirin if not contraindicated should also be considered. Being seen by a preventive cardiology specialist to make sure you are on the right path should be considered.
LDL and LDL Particles
Imgaiso: Can you share your personal opinion on whether test such as LDL particle number, LDL size, and HDL size are of value? If so, do you prefer NMR or VAP?
Dr__Stan_Hazen: Importantly, LDL (bad) cholesterol is not the whole story. A comprehensive preventive cardiology program aim to reduce cardiac risk by taking a global approach - with each thing providing additive, independent value. This means focusing on not just LDLc (that is the major target to hit) but also, other lipid risk factors (TG, HDL), blood pressure control, platelet/anti-thrombotic targeted therapy as long as not contraindicated, diabetes control, weight reduction, looking for inflammation/chronic diseases that are associated with cardiac risks, exercise program (this includes the full course of cardiac rehab with each and every event/revascularization procedure), checking thyroid, nutrition approaches, etc.
There is evidence to support the concept that being at "goal" with LDL cholesterol alone often isn’t enough - especially in those with elevated "non-HDL cholesterol. This is a calculated number (total cholesterol - HDLc), and is actually part of national guidelines.
Lipoprotein subparticle fractionation helps get at this (elevated non-HDL cholesterol elevation. Perhaps the best data is available for measurement of LDL particle number (LDLp). After looking at LDLc goal, I think it reasonable, even though not part of national guidelines yet, to make sure the LDLp is not still elevated (or that non-HDL cholesterol isn’t elevated). This comes into play more often than not where triglycerides are elevated, so some of these measures are interrelated. An apolipoprotein B level provides virtually identical information to an LDLp. If either is elevated, more aggressive lipid lowering (i.e. higher statin dose, or more potent statin) may provide added benefit. As for LDL size - that value is integrally tied into LDLp and one should either focus on one or the other…and LDLp (or apoB) seems to be the best to focus on.
As for HDL size…. While there are some that use it, I personally have not yet been persuaded by the literature. I have yet to see the data to support this at the present time. This is not to say that I don’t believe a future HDL related test will emerge as being important. I think there will be new tests for HDL that both monitor function instead of mass, and that quantify the "dysfunctional" HDL level….but neither of these are available at the present time for clinical use.
Finally - as for NMR vs. VAP - I think 90-95% of the time, a simple lipid profile is all that is needed. When looking to more specialized lipoprotein testing, I think the question shouldn’t be NMR vs. VAP, but apoB vs. NMR vs. VAP. I personally prefer apoB because there is more data to support it, it is simpler, faster, and cheaper at the present time within my institution. I am unaware of any convincing data to claim superiority of apoB vs. LDLp (NMR). My current read of the literature is that there is more data to support either of those vs. subparticle fractionation by VAP.
Imgaiso: Should high Lp(a) be treated?
Dr__Stan_Hazen: Yes. high Lp(a) is a clear risk factor for cardiac disease and adverse events (MI, stroke, death). Our national guidelines are behind on this one. LP(a) is considered in national guidelines in other countries, we haven’t caught up on this yet. We and others have convincingly shown that Lp(a) is both a marker and genetic mediator of increased cardiac risk. When elevated (e.g. >30 mg/dL protein), I recommend more aggressive LDL goals. In fact, in a recent study of over 5000 subjects seen in Preventive Cardiology Clinic at CCF, we observed that overall mortality was increased in those with LP(a) >30. But if the LDLc achieved was <70, the incremental increase in overall mortality was negligible. For this reason, when LP(a) >30 is observed in clinic, we aim for the more aggressive LDL goal of <70.
We also are more likely to focus on stroke prevention with high Lp(a) - including closer attention to BP goals, and a push for low dose aspirin prophylaxis therapy, unless there is a clear contraindication like prior history of GI bleeding, ulcers, or other GI issues with aspirin.
Now - you will note I didn’t say "treat" the LP(a). But instead, to be more aggressive with other preventive measures, including lower LDLc goals). That is because Lp(a) levels are genetically wired, and don’t change much. Once Lpa is seen to be high, we don’t repeatedly monitor it. At present, our current medications don’t make significant changes in Lp(a) levels. Only niacin helps to lower it (modestly). I would prefer a patient be on a statin to lower LDL as opposed to niacin simply to lower Lpa. The data for reduction in cardiac events is strongest in statin therapy.
Lp(a) levels are highly related to genetics, and it is hard to change one's level. But it seems that lowering the LDL level (the particle that the LP(a) binds to in the blood) helps to lower the risk associated with elevated levels.
barjoyner: I have very good normal Lipid -C panels but very very high LDL-P numbers (2123) and very small LDL particles size (1117) . I also have family history of heart disease. How important is this marker and does it respond to plant based diet?
Dr__Stan_Hazen: The primary goal is to reduce LDLc to below goal. For primary prevention subject (no known heart disease or diabetes) we recommend a minimal LDL of < 100. If additional risk factors are present, while not part of national guidelines, we often opt for a more aggressive goal of < 70. In subjects with strong family history of heart disease, we look at markers like LPa to see if they are elevated, and if so, then opt for < 70 as the LDL goal.
Once LDL is at goal, if LDLp (LDL particle number) remains high, then data suggests there is residual risk, and more aggressive lipid lowering may be beneficial, along with focus on efforts to bring TG, weight loss and insulin resistance in check. Lifestyle and dietary efforts do become more important in helping to bring high LDLp down when LDLc is at goal. A routine exercise program can help significantly, as well as losing just a few lbs.
As for the very strict vegan diets - while they can be healthful, they are very difficult to adhere strictly to, and trial data with them is rather limited. So I am less inclined to push dogmatically for a strict vegan diet, and to instead recommend do what you can within reason. A vegan diet per se does not reduce LDLp specifically. But it does tend to be very low in cholesterol, higher in fiber, and lower in fats and carbohydrates - all things that help to reduce LDLc and LDLp, and improve glycemic control. Adopting a routine exercise program is just as important, and provides additive cardiovascular benefits. This can mean just walking at a brisk pace 30-45 min daily.
janpersico: With an Lpa of 170, LDL of 58, HDL of 43, good BP, Hx of MI, cardiac stents and carotid stent. Good diet and exercise program. What else can I do to mitigate the high Lpa
Dr__Stan_Hazen: You probably are already on it - but low dose aspirin (2 x 81 mg) can help reduce risks and is recommended provided there is no contraindication (GI issues, bleeding). With an LDL at that level, you likely are on a statin. If not, I would recommend looking at your regimen to try and put you on one. BP control is also important (1230/80 goal).
Also - with high LPa - your siblings and children should be screened. heart disease runs in families, and LP(a) is highly heritable.
Novel Cardiovascular Risk Markers
Imgaiso: Are any novel markers of any value in your opinion?
Dr__Stan_Hazen: Yes. Here are a few I think are of value. It is not exhaustive - just the highlights:
1) High sensitivity (hs) CRP - this marker of inflammation is a good prognostic indicated of cardiac risks. If elevated, even with "normal" LDL (i.e. LDL < 100), there is trial data to support starting a statin (even in those without known cardiac disease). The Jupitor trial looked at nearly 20,000 subjects and started a high potency statin vs. placebo in those with normal LDL if their CRP was elevated.
Those taking the statin had up to 40-50% reduction in events, and the trial was stopped prematurely because it was felt unethical to continue it further because the benefits were so dramatic.
Other studies show that even if at "goal" with LDlc, if hsCRP is still high, there is residual cardiac risks. For this reason, we still on occasion check CRP periodically to see if more stringent risk reduction efforts should be considered.
2) MPO (myeloperoxidase) - this is another inflammation marker that is linked to development of "vulnerable plaque" - heart attack, or death risk. An elevated level also is associated with future risk of developing heart failure. When elevated, it predicts cardiac risks independent of traditional risk factors. It also is independent of CRP.
There are no intervention studies with elevated MPO at present (other than CRP, there aren’t any for most new markers). However, given the number of studies that keep showing increased risks, if elevated, we recommend more globally aggressive risk reduction efforts. This includes selection of lower LDL goals that otherwise might be recommended by national guidelines, consideration of low dose aspirin, and adoption of more aggressive preventive lifestyle efforts (diet, exercise, weight reduction).
3) NT-proBNP (or BNP) - this is a cardiac marker of stress (actually - stretch/strain of the heart). Many studies have shown it is elevated in heart failure, but more recently, it also has been shown to predict increased risk for development of cardiac disease in middle aged apparently healthy subjects, or progression of cardiac disease. When elevated, we focus on blood pressure control and heart failure preventive efforts. We also are more globally aggressive with lipids and other risk reduction efforts.
4) Urine albumin/ creatinine ratio - this is a marker of early atherosclerosis in the kidneys, and a risk for cardiac disease. Many studies have shown it is elevated in subjects with diabetes (it can become an early marker of kidney injury from diabetes too), but more recently, it also has been shown to predict increased risk for development of cardiac disease, even in otherwise apparently healthy subjects. When elevated, we focus on blood pressure control with certain classes of BP medications that help protect the kidneys (ACEI or ARBs). We also are more globally aggressive with lipids and other risk reduction efforts.
5)Homocysteine - this is an old marker of risk but recent studies have brought it back into consideration. When elevated, even in subjects with normal kidney function and no other clear risk factors, it predicts increased risk. This is a personal opinion - but I believe in a primary prevention subject, there is a place to on occasion check a Hcys. Because if elevated, it heralds increased cardiac risks. So if there is ambiguity in whether to start a person on medication for preventive efforts, I sometimes check a Hcys to see if the results will tip me more in favor of recommending a statin, vs. not. Again - this is not part of national guidelines - but there data is pretty clear that elevated Hcys levels are predictive of increased risk. The question becomes - what to do with it if seen. I think it prudent to be more globally aggressive with common sense efforts (BP control, LDL levels, diet, exercise, weight control). I do not chase after Hcys levels. Just check it once to see where things stand if there is ambiguity as to whether to start a medication or not.
Peppy: If gut flora is responsible for some individual's plaque burden, should they begin taking a probiotic? Which one?
Dr__Stan_Hazen: Unfortunately, we don't know of any commercial probiotics yet that are "heart healthy". The best thing at this point is to try and reduce the substrate (animal products) - so a low fat low cholesterol diet works out pretty well. No choline or lecithin supplementation is recommended.
azdi: What to do since I have high cholesterol (>300) and get myalgias from statins? I must not be the only one in this situation. 64 y/o female with zero calcium score and totally clear angiogram. No other risk factors. Exercise, eat Mediterranean, BMI 22, good BP, etc. Low crp and Lp(a). Don't know particle size.
Dr__Stan_Hazen: Having such a high cholesterol does increase the risk of cardiac disease. While having a normal calcium score and angiogram are good signs, they do not absolutely indicate that you do not have risk. Up to 20% of events occur in subjects with a normal calcium score, and the site of heart attack occurs >50% of the time where there is little narrowing (stenosis is < 50%).
With statin intolerance, such as you have, it is often possible to still bring about significant LDL cholesterol reduction. Side effects are dose dependent. We typically can help bring about an additional 30% LDL reduction in subjects with statin intolerance by both using low and infrequent dosing of longer acting statin (e.g. use of a pediatric sized dose, once a week) in combination with additional cholesterol lowering approaches. Some of these include use of cholesterol absorption blockers (e.g. plant sterols, or zetia) or alternative lipid lowering agents that do not cause as many issues with muscle aches/fatigue.
Imgaiso: Currently I take a statin. The statin reduced my LDL down to 39 and my HDL to 34. On a reduced dose of the statin my LDL was 57 and HDL was 51. So, the reduction increased both LDL and HDL on a one-for-one basis. That is, the reduction increased LDL by 18 and HDL by 17. Which is the better profile in your view (A) LDL = 39 and HDL = 34 or (A) LDL = 57 and HDL = 51?
Dr__Stan_Hazen: Hard to say - both are fantastic. If you have known CVD, I like the first one (Lower LDL). As long as you weren’t having side effects from the medication. If you are primary prevention - either is fine
Imgaiso: Do you think that statins have a CVD benefit besides reducing cholesterol?
Dr__Stan_Hazen: Yes – definitely. If one looks at the risk for cardiac events vs. LDL level, the curve appears to he "J shaped" - i.e. - as LDL gets lower, the risk flattens out - but if one instead looks at risk reduction from statin induced LDL lowering, the curve appears linear (i.e. - lower LDL = lower risk). Also - look at stroke risk for example. There is only a weak association between LDL and stroke risk . But taking a statin has a fantastic stroke risk reducing intervention (far more so than predicted by LDL curve vs. stroke risk). Many lines of evidence point toward inflammation being mechanistically linked to plaque vulnerability and statins helping to "pacify" inflammation in the artery wall.
Bottom line - if a subject has known cardiac disease (atherosclerotic plaque) - even if LDL is <100 (or lower) - if not on a statin, I recommend one.
cohnanita: which statin is less connect to myalgia?
Dr__Stan_Hazen: All statins are equivalent with respect to muscle aches. All are dose related with respect to side effects.
Imgaiso: Do you believe that fish oil or fish consumption is valuable for primary prevention?
Dr__Stan_Hazen: Yes. I do. The data supports this too. A diet with at least 2 portions of fish (cold water varieties, like mackerel, sardines, salmon, herring), which are high in omega 3 fatty acids, is associated with decreased cardiac risks. This may have as much to do with replacing less healthy foods with the healthier choice of the fish. Clinical studies have shown reduction in cardiac risks with omega 3 fatty acid supplementation.
Aim for at least 1000 mg omega 3 FA. Ideally, 2000 mg (can be taken at same time with any meal). It is important to add up the EPA + DHA on the label to = 2000. These are the omega 3 fatty acids. Some fish oil supplements are simply extracts of the blubber of a fatty fish that is low in omega 3 FA. SO it is important to read the label. As a general rule, you should be able to get 2000 mg in 2-3 capsules (some capsules have so little EPA or DHA that it can take 7 or more to get 2000 mg).
In subjects with elevated marker of inflammation, or in those with inflammatory diseases associated with cardiac risks, like rheumatoid arthritis, or SLE, we also suggest omega 3 FA supplementation, because they can have anti-inflammatory effects (this may in part be how supplementation helps reduce cardiac risk).
janpersico: Post menopausal women with hx of CVD, and family hx of history of CVD, what is the need for calcium/vitamin D supplements, with osteopenia?
Dr__Stan_Hazen: The decision for Ca supplements and Vit D should be based solely on the Vit D and osteopenia workup. The data out there on Ca supplements and cardiac issues is confusing - while some risks have been seen, other studies have suggested benefit. The bottom line is, if there is a risk or benefit from CVD standpoint, it is likely very modest. Against that is the real risk of hip fracture or compression fractures of the spine - both of which significantly reduce freedom/mobility, and are associated with considerable morbidity and even mortality risk.
paulyim: You recommend Omeg3 FA and how about Vit.E?
Dr__Stan_Hazen: The data on Vitamin E suggests it does not provide added benefit for most subjects. There are a few subpopulations where Vitamin E may be helpful - those with known renal disease, and those with heart transplants. In each subgroup, randomized trials have shown benefit (for retarding heart disease in kidney patients, and for reducing transplant arteriopathy in transplant subjects).
There is research data that a subset of diabetics may benefit from Vitamin E depending on the subtype of their haptoglobin. This is a research only at present - and we do not recommend Vitamin E routinely in subjects with diabetes. Lastly, a recent intervention study showed benefit from Vitamin E for subjects with NASH (non-alcoholic steatohepatitis). We therefore recommend Vitamin E supplement for that subset of subjects also.
Cardiovascular Risk Prevention in the Elderly
bhakta: All questions are with respect to geriatric patients.1. Does Candesartan offer any additional benefit over Losartan in reducing cardiovascular risks?2. What supplements would you recommend in a geriatric patient? Do either of these supplements help? And in what dosage? A) CoQ-10. B) Omega-3. C) Resveratorol. D) D-Ribose 3. How would you treat Isolated systolic hypertension. Approximate diastolic BP = 60 and systolic = 150+
Dr__Stan_Hazen: Candesartan and losartan are not supplements - they are antihypertensive drugs in the family of ARBs (Angiotensin Receptor Blocking agents). They are both reasonable agents for BP control, and as a class, ARBs (like ACEI - angiotensin converting enzyme inhibitors) provide added benefits for diabetics, and anti-atherosclerotic effects perhaps in addition to simple BP lowering.
For a geriatric patient, most important is a healthy balanced diet. Osteoporosis targeted supplements (calcium supplements if needed, checking vitamin D and supplementing if needed) is more important. Otherwise, we recommend no specific supplements in geriatrics (best to get nutrients in food/vegetables/fruits).
CoQ10 is a nutrient that can be reduced in some subjects that are taking statins. We only recommend this supplement if one is experiencing muscle aches or fatigue potentially attributable to the statins. Up to 50% of subjects with statin related muscle issues have reported improvement when taking coQ10 supplements. We recommend 200 mg daily with food in this situation (regardless of age) as a trial to see if it helps (with statin related muscle issues).
Omega 3 FA help to lower TG levels. They also have been shown to reduce heart disease risks. In subjects with TG elevations, we recommend 2000 mg omega 3 FA. If TG is significantly above goal (<150) despite 2000 mg, the dose can be increased to 4000.
Candesartan and losartan are not supplements - they are antihypertensive drugs in the family of ARBs (Angiotensin Receptor Blocking agents). They are both reasonable agents for BP control, and as a class, ARBs (like ACEI - angiotensin converting enzyme inhibitors) provide added benefits for diabetics, and anti-atherosclerotic effects perhaps in addition to simple BP lowering. For a geriatric patient, most important is a healthy balanced diet. Osteoporosis targeted supplements (calcium supplements if needed, checking vitamin D and supplementing if needed) is more important. Otherwise, we recommend no specific supplements in geriatrics (best to get nutrients in food/vegetables/fruits). CoQ10 is a nutrient that can be reduced in some subjects that are taking statins. We only recommend this supplement if one is experiencing muscle aches or fatigue potentially attributable to the statins. Up to 50% of subjects with statin related muscle issues have reported improvement when taking coQ10 supplements. We recommend 200 mg daily with food in this situation (regardless of age) as a trial to see if it helps (with statin related muscle issues). Omega 3 FA help to lower TG levels. They also have been shown to reduce heart disease risks. In subjects with TG elevations, we recommend 2000 mg omega 3 FA. If TG is significantly above goal (<150) despite 2000 mg, the dose can be increased to 4000. In secondary prevention (patients with known heart disease) we often also recommend omega 3 FA supplementation (2000 mg). This is because randomized trials have shown added risk reduction on top of standard care in several trials. It is important to read the label for "fish oil". The blubber of a white fish doesn’t always have high omega 3 FAs (the healthful fatty acids). EPA and DHA are the omega 3s. The goal of 2000 mg should be the total of the EPA + DHA , and should be able to be achieved with 2 or 3 capsules. Isolated systolic hypertension should be treated. Goal BP is 120. Resveratrol - the jury is out on this still. Large prospective placebo controlled randomized trials are lacking. We do not recommend it at present. and are hoping more data will come out over time. D-Ribose - even less is available. I do not recommend it.
Peripheral Artery Disease
MichaelC: Is it possible to have Peripheral Artery Disease without having a trace of Coronary Artery Disease (as determined by an angiogram)? My measured total cholesterol from 2003 to 2009 has been 141, 145, 149, 155, 159, 150. My age is 61.
Dr__Stan_Hazen: Yes - peripheral artery disease (PAD) often is a sign of systemic (throughout the body) vascular disease (atherosclerosis). But in a smaller subset, it appears to be rather isolated. Even so, the risk for heart attack, stroke and death still is increased in PAD subjects (similar to heart disease patients that have already had one heart attack). For this reason, national guidelines recommend very aggressive preventative approaches with PAD subjects, including LDL goal <70, statin therapy, aggressive BP control, low dose aspirin, etc. Even with low TC as you noted, I would recommend a statin in the setting of documented PAD.
It is particularly important to try and adopt an exercise program with PAD. Pushing the exercise to the point (and past) of leg pain on a regular basis has been shown to help improve circulation and walking distances long term in subjects with PAD. The vessels will grow, and can make new connections if the body keeps repeatedly sensing need for growing more vessels (the leg pain is oxygen debt to the muscle).
Imgaiso: What do you think of ultra low fat diets? Do they have a benefit beyond lowering cholesterol?
Dr__Stan_Hazen: I am not a fan of "ultra" any type of diet - just a well rounded, prudent heart healthy one - such as what is recommended by the American Heart Association. Only time I push for "ultra" strict diet restriction is a low salt/sodium diet for someone with heart failure. Otherwise, it is a general low fat, low cholesterol diet that is recommended. You have to live - and a prudent diet, with occasional treats (in small portions) seems totally reasonable.
Coronary artery Disease
tonycep: I have an obtusive marginal artery that is 100% blocked. The artery could not be successfully opened. How significantly is this. I do have a lot of colateral flow.
Dr__Stan_Hazen: Unfortunately, sometimes smaller or harder to reach vessels may be difficult to stent, and if the area at risk is modest, and good collaterals present, the decision made to opt for medical alone rather than medical + revascularization. This simply means you have known heart disease, and should be treated aggressively. The same as if you had been stented. Undergoing a cardiac rehab program is recommended to help in developing a safe exercise program.
Walker: When a (Right) Coronary Artery is blocked are there other alternatives other than Stent / Angioplasty and medications (such as Plavix & Carvedilol) that should be considered especially when a patient has experienced Systemic Scleroderma? It is assumed that there are higher risks based on the probable hardening of heart muscle tissue and vascular tissue. Does proceeding with a Stent preclude any options in the future? Any reasons not to do a Stent? (No Angina being experienced and walking 3-5 miles per day.)
Dr__Stan_Hazen: This is a complicated situation and really needs to be discussed with a preventive cardiology/cardiology specialist.
Cleveland_Clinic_Host: I'm sorry to say that our time is now over. Thank you again for taking the time to answer our questions about cardiovascular risk factors.
This information is provided by Cleveland Clinic as a convenience service only and is not intended to replace the medical advice of your doctor or health care provider. Please consult your health care provider for advice about a specific medical condition. Please remember that this information, in the absence of a visit with a health care professional, must be considered as an educational service only and is not designed to replace a physician's independent judgment about the appropriateness or risks of a procedure for a given patient. The views and opinions expressed by an individual in this forum are not necessarily the views of the Cleveland Clinic institution or other Cleveland Clinic physicians.
Talk to a Nurse: Mon. - Fri., 8:30 a.m. - 4 p.m. (ET)
Call a Heart & Vascular Nurse locally 216.445.9288 or toll-free 866.289.6911.
Schedule an Appointment