Thursday, December 21, 2006

My Triple Bypass Surgery Part III

My Triple Bypass Surgery Part III

Dear Ones! Hari OM !

Here are some of the links that may enlighten you about this CAD - Coronary Artery Diseases - Problem
1. About Heart
2. About bypass Surgery
3. This may be good info but it may be an AD.
4. Heart attacks among Indians.htm - Already attached belowe. If you cannot open the graphs and charts and tables, please let me know, I will send you a file that has that already open and also pdf version. It is about three MB size, so make sure that you can receive it.
5. What to do in Emergency while going through Heart Attack - Power Point presentation. Attached herewith.
6. Learn CPR

In my case:

1. CMC Manchester had inserted Catheter through right groin area, for analyzing the problem. Also used Ultrasound to access the size of the blockages.

Washington Hospital Heart Center:

2. They put some needle set up for drawing Blood and introduce fluid / IV. They had one on my forearm and one on my neck.
The line in your neck is called a central line, a special IV (intravenous) for giving medicines. In my forearm was either a peripheral IV or a radial arterial line to invasively monitor BP constantly
3. They use fine saw to cut Sternum into half, to open the rib cage and keep it open for the duration of Surgery. That would put lots of strain, stress on involved muscles, ligaments etc.
4. Artficial Heart-Lung Pump was not used in my case?
Usually, The heart-lung machine puts additional strain on the heart because the heart is stopped.
5. Triple Bypass
· An artery was detached from the chest wall called - Left internal mammary artery or LIMA and the open end was grafted to the coronary artery below the blocked area. He by passed three blockages with this one. This involved a loop to jump across to another artery, hence, two.
· A piece of a long vein from my right leg was taken to by pass the old two stents, so as to avoid any complications of stents as heart area was open anyway. This is the third one.
· One end is sewn onto the large artery leaving your heart -- the aorta. The other end of the vein is attached or "grafted" to the coronary artery below the blocked area.
· Either way, blood can use this new path to flow freely to the heart muscle.
6. They put two tubes connected to suction pump, to continue collecting the fluid. It was taken off after a couple of days.
7. Catheter was introduced to connect to urinary bladder, which was also pulled out after a couple of days. .

OM Namah Shivay OM ! Sudhir

An Illustrated Guide to Understanding and Reducing Your Risk of A Heart Attack at a Young Age Enas A. Enas, MD, FACC the former having the highest and the


It appears that Asian Indians and chinese are at the opposite end of the CAD spectrum, with the former having the highest and the latter having the LOWEST rates of CAD"

The high rates of CAD in Asian Indians worldwide are accompanied by paradoxically low rates of conventional risk factors, such as smoking, high blood pressure and high Cholesterol. "

"Diabetes, together with the metabolic syndrome, accounts for a third of the excess burden of CAD among Asian Indians."

"Lipoprotein (a) level in Asian Indians are 5 – fold higher than American Indians and 2-fold higher than Whites."

Lipoprotein (a) is at least 5 times as dangerous as LDL in its ability to produce an early heart attack or Stroke."

"In Asian Indians, the adverse effect of elevated Lp (a) is markedly increased, by low level of HDL, high levels of LDL, triglycerides, and homocysteine."

"The risk of a heart attack may be increased 122 – fold, when high levels of Lp (a) coexist with high TC/HDL ratio, homocysteine, and any one of the usual risk factors – smoking, diabetes, or high Blood Pressure."

"AN increase in blood Cholesterol level of 10 mg/dL among Asian Indians appears to have the same impact as an increase of 40-50 mg/dL in other populations."

"Among Asian Indians , the CAD risk with Cholesterol level of 160 mg/dL is similar to that of Americans with Cholesterol Levels of TC 240 mg/dL."

“Waiting until chest pain to take proactive action against an early heart attack, is as foolish as waiting for labor pain to begin prenatal care.”


Magnitude of CAD among Asian Indians

Asian Indians have the highest rates of coronary artery disease (CAD), irrespective, of region, religion, gender, and education. These rates include incidence (new cases per year), mortality, and prevalence (the percentage of people alive with the disease). The CAD mortality rates vary more than 10-fold in men and women worldwide. CAD rates in a given country was once thought to be related primarily to the affluence and the size of its economy, as happened in the United States (U.S.) 50 years ago. Despite having the second and third largest economies, the Chinese and the Japanese have had the lowest rates of CAD, on international comparison (Graph_1), both having rates 4-fold lower than Americans.

(The conspicuous absence of India is due to lack of such national data on CAD) Graph 2


Graph 3 show the mortality rates among Asian Indians in comparison to other populations in
various countries.

Asian Indians with the fourth largest economy have a 4-fold higher rate of CAD than the US , the world's largest economy (Graph 4).

Graph 5 shows the 3-fold higher incidence of CAD among Asian Indians in Singapore .

Graph 6 shows a 6-fold higher rate of hospitalization (an indirect measure of incidence and prevalence) for heart attack, coronary angioplasty, and bypass surgery among Asian Indians than Chinese in the U.S. It appears that Asian Indians and Chinese are at the opposite end of the CAD spectrum, with the former having the highest and the latter having the lowest rates of CAD. The term Asian Indian refers to all those who trace their origin to the four countries in the Indian subcontinent - India , Pakistan , Bangladesh , and Sri Lanka .

CAD Rates among Asian Indian Women: The excess risk of CAD in Asian Indians is even greater in women than in men, despite the fact that tobacco abuse is virtually non-existent among these women (Graph 3).

Asian Indian women have a higher death rate from CAD than women of all other ethnic origins in the U.K. , South Africa , Canada , Singapore , Fiji , Mauritius , Uganda , and Trinidad . Although national data in the U.S. are not available, a similar phenomenon was reported from the state of California . Women develop CAD about 10 years later than men, but the prognosis of women with CAD is worse than men.

CAD Rates in India : During the past 3 decades, the average age of a first heart attack increased by 10 years in the U.S. , but decreased by 10 years in India . About 50% of all heart attacks among Asian Indian men occur under the age of 55 and 25% under the age of 40, unheard of in any other population. Also during the same period, CAD rates increased 3-fold in urban India and 2-fold in rural India . Ironically, this increase happened at a time when the CAD mortality rate declined by 54% in the U.S. as shown in Graph 7.

Currently, the prevalence of CAD in urban India is double the rate in rural India and 4-fold higher than in the U.S, which has an enviably low prevalence of only 2.5%. The CAD rates in urban India are similar to those among the generally more affluent overseas Indians. For example, the prevalence of CAD in New Delhi is 10% and Chennai 11%. The rates appear to be highest in Kerala (despite its highest literacy), where prevalence of CAD is 13% in urban areas and 7% in rural areas.

Ethnic Differences in Heart Attack and Stroke: The predominant form of cardiovascular disease is myocardial infarction or heart attack among Europeans and Americans, whereas it is stroke among Asians. Asian Indians are unique in having high rates of both stroke and heart attack. The underlying process in the vast majority of both these conditions is a disease process called atherosclerosis or hardening of the arteries. A gradual narrowing of coronary arteries over years (Picture 1) result in a characteristic chest pain called angina.

A sudden occlusion from a blood clot in an artery supplying vital areas in the heart results in a heart attack (Picture 2).

A similar occlusion in the brain results in a brain attack or stroke, which is a painless but debilitating condition. Such blood clots are almost always the result of the rupture of a young, soft, cholesterol-rich, and calcium-poor vulnerable plaque (Pictures 3

and 4)


The Paradox of Greater Risk of a Heart Attack with Less Narrowing of Arteries: Contrary to common wisdom, we now know that most heart attacks occur at sites with mild narrowing and not severe narrowing of coronary arteries. For example, only one in five of the heart attacks occur in sites with severe (>75%) narrowing, whereas almost half of all heart attacks occur with mild (<50%)>240 mg/dL. It is estimated that about 50% of Asian Indians have metabolic syndrome compared with 25% among other Americans. Metabolic syndrome and diabetes, however, cannot explain the excess burden of CAD among Asian Indians, because all minorities in the U.S. , including Blacks and Hispanics, have high rates of diabetes but low rates of CAD. The other risk factors of greater importance in Asian Indians are given in Table 3.

Cholesterol Made Easy - the Good, Bad and the Deadly
Although cholesterol is generally considered bad, not all the cholesterol in the blood is bad. The blood cholesterol consists of the "good cholesterol" or high-density lipoprotein (HDL),"bad cholesterol" or low-density lipoprotein (LDL), ugly cholesterol or very low density lipoprotein (VLDL) and the deadly cholesterol or lipoprotein(a) {Lp(a)}. The optimum levels of various cholesterols are shown in Table 4.

Good Cholesterol: HDL actually protects against heart attack; the higher the blood level of HDL, the lower the risk of heart attacks. Although not considered low, an HDL level of 45 mg/dL has a 2-fold and 25 mg/dl has a 4-fold risk of a heart attack compared to 65 mg/dL as shown in Graph 10.
In the Framingham heart study, those with HDL <40>260 mg/dL. HDL level is about 10 mg/dL higher in women than men worldwide. The optimum HDL level is 65 mg/dL, which is seen in Black, Chinese, and Japanese women. No wonder why they have low rates of CAD. The average HDL level is 55 mg/dL in White women and 45 mg/dL in White men. The HDL level among Asian Indians are about 5-10 mg/dL lower than Whites and 15-20 mg/dL lower than Blacks as shown in Graph 11.

The low HDL among Asian Indians results in high total cholesterol/HDL (TC/HDL) ratio, which is a powerful predictor of CAD risk in diverse populations. In the Quebec Cardiovascular Study, persons with TC/HDL ratio of >5 had a 2-fold higher risk of CAD than those with a ratio of <4.>5. In the CADI Study, 62% of Asian Indian men had high TC/HDL ratio, though only 20 % had high cholesterol levels (Graph 12)

Whereas high TC/HDL ratio >5 identifies more Asian Indian men, HDL<50>160 mg/dL.

Bad cholesterol: LDL is the true cholesterol villain that clogs up the coronary arteries. Newborns worldwide have an LDL of 35 mg/dL but LDL rises gradually in childhood depending primarily on the intake of saturated fat. Once the LDL level exceeds 80-100 mg/dL, it begins to be deposited inside the coronary and other arteries. This process often starts during the childhood, progresses silently for decades and presents as a cardiac catastrophe in the form of a massive heart attack or cardiac arrest but rarely as chest pain. The relationship of increasing risk of a heart attack with increasing levels of LDL and decreasing HDL is shown in Graph 13.
Ugly cholesterol: Emerging data strongly indicate that a triglyceride level >150 mg/dL is an important risk factor, especially in women (Graph 14).
Triglyceride levels are related to VLDL, which is usually 20% of the total triglycerides. High triglyceride levels make the LDL small, dense, and dangerous. Therefore, I use the term "ugly cholesterol" to describe triglycerides. Most individuals with high triglyceride levels develop diabetes in 5-10 years. The lowest risk of CAD is among those with triglyceride levels <50>20 mg/dL, the usual cut point for elevated Lp(a). Several recent studies in India , among patents with CAD under 40 years of age, have shown high levels of Lp(a) among 50-60% of patients and was the only risk factor in 30-40% of cases.

Although Blacks have the highest levels of Lp(a), the atherogenic effects of elevated Lp(a) are significantly mitigated by an otherwise anti-atherogenic lipid profile (high levels of HDL and low levels of triglycerides, and LDL). Conversely, the pathological effects of elevated Lp(a) are exponentially increased in Asian Indians, as a result of a highly atherogenic metabolic milieu, consisting of high levels of triglycerides, apolipoprotein B, homocysteine, glucose, plasminogen activator inhibitor-1, fibrinogen, C-reactive protein, and low levels of HDL, especially HDL 2b. More than a third of the Asian Indians have atherogenic levels of most of these emerging risk factors.

Multiplicative Effects of Emerging and Conventional Risk Factors: It is well known that diabetes not only increases the risk of a heart attack but also has a multiplicative effect with other risk factors. At any given level of cholesterol, the CAD risk is 3 to 4-fold higher among diabetic patients than non diabetics, as shown in Graph 16.

It is often not appreciated that the increased risk of a heart attack and stroke from high levels of Lp(a) is much greater than from diabetes. For example, high Lp(a) levels can increase the risk of CAD from other risk factors by as high as 10-fold, compared to only 4-fold with diabetes. The impact of high levels of Lp(a) in increasing the risk of a premature heart attack from other risk factors is shown in Graph 17.
More importantly, the risk of an early heart attack is greater with high TC/ HDL ratio than with high cholesterol as shown in Graph 18.

As an extreme example, the risk of a heart attack may be increased by 122-fold, when high levels of Lp(a) coexist with high TC/HDL ratio, homocysteine, and any one of the usual risk factors (smoking, high blood pressure, or diabetes). Thus Lp(a) is one of those rare factors, that can make 4 and 4, not 8 or 16, but 64 and beyond The estimated contribution of various risk factors to CAD among Asian Indians is given Graph 19.

Double Jeopardy from Nature and Nurture: These multiplicative effects of conventional and emerging risk factors appear to provide a plausible explanation for the excess burden of CAD among Asian Indians, many of whom are lean, nonsmoking, vegetarian, yoga guru, and marathon athletes. Further elucidation of the precise role of the multiplicative effects of other emerging risk factors in Asian Indians is urgently needed to develop appropriate preventive and therapeutic strategies. Selected factors related to nurture that make Lp(a) most dangerous are shown in Table 5. Since nature cannot be altered nurture should be attacked much more vigorously.

Why Asian Indians Should be Treated Differently

Lessons from Singapore : A study of cord blood in about 1000 newborns in Singapore has shown higher levels of Lp(a) among Indians than Chinese that parallel the adult difference in CAD rates. Singapore was the first country to report a 3-4- fold higher rate of CAD among Asian Indians compared to Chinese, nearly 50 years ago. During the past 30 years, the overall rate of CAD doubled in Singapore due to changes in diet and lifestyle. But a 3-fold difference in CAD rates between Indians and Chinese was maintained. Because of the genetic susceptibility, the adverse effects of conventional risk factors related to adverse lifestyle such as smoking, high blood pressure, high cholesterol, and diabetes are markedly magnified. It appears that increase in CAD risk from a weight gain of 10 pounds or smoking 10 cigarettes (or beedi) by Indians is similar to a 30 pound weight gain or smoking 30 cigarettes by other populations. More importantly, an increase in blood cholesterol level of 10 mg/dL among Asian Indians appears have the same impact as an increase of 40-50 mg/dL in other populations.

The database to support treatment recommendations is derived primarily from studies of White populations. The risk of CAD from all known risk factors is graded and continuous but genetic factors determine individual variations in disease susceptibility in response to environmental factors. For any given level of risk factors, the CAD risk among Asian Indians is at least double that of Whites. Therefore, the threshold of intervention and goals of treatment should be lower in Asian Indians than in Whites by 10% to 20%, akin to those recommended for patients with diabetes.

In the NCEP III, diabetes is regarded as a CAD risk equivalent, with an LDL goal of <100>40% of Asian Indians have high levels of Lp(a) and >90% have low levels of HDL 2b (the best of the good cholesterol), lowering LDL to <80>30%, and selectively increases the cardioprotective sub-fraction of HDL by >40%. It can be given safely in combination with statins. A new combination of Niaspan and lovastatin (Advicor) has just been introduced in the U.S. In postmenopausal women, estrogen replacement therapy can lower Lp(a) by 30-50%. In the Heart and Estrogen/Progestin Replacement Study, the risk of a recurrent heart attack was reduced by 50% among women with elevated Lp(a) without any harm whatsoever. Vitamin preparations containing folic acid, B12, and B6 (Foltx, Folgard, Folic Acid Extra) can substantially reduce elevated homocysteine levels and is advisable in those with homocysteine levels >10 micromol/L.


India is currently in the middle of a CAD epidemic that was initially observed and not yet abated among overseas Asian Indians. Although the conventional risk factors do not fully explain the excess burden of CAD, these risk factors are doubly important in Asian Indians, and remain the principal targets for prevention and treatment. Due to the genetic susceptibility mediated primarily by elevated levels of Lp(a), the adverse effects of the conventional risk factors are magnified several-fold. Therefore, the threshold of intervention and goals of treatment for various risk factors in Asian Indians should be 20% lower than Whites for LDL and 10% lower for all other risk factors (Tables 2 and 4).

It seems appropriate to begin preventive strategies at least 20 years earlier than in other populations (men 25 and women 35 years of age) because of the extreme pre-maturity and malignant nature of CAD. The benefit of statin therapy appears to far exceed that of treatment of hypertension, the impact of which is primarily on lowering the risk of a stroke. Therefore, lipid-lowering therapy with statins should be considered among the first line of treatment rather than the last thing we do. Remember, waiting until chest pain to take proactive action, against an early heart attack, is as foolish as waiting for labor pain to begin prenatal care. Daily exercise, avoidance of tobacco, and reduced intake of saturated fat could reduce both the need and the dose of medications and the importance of these measures cannot be overstated.

This article is a synthesis of the research findings and opinions of the author. It is not intended for instituting treatment, without careful evaluation of the individual risk and benefits. Treatment decisions on the use of medications must be made by a physician qualified and licensed to practice medicine in the respective geographical area. This article cannot be republished without written permission of the author.

For List of Reference Articles, see publications authored by Dr. Enas A Enas @

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