Munich, Germany - A new prospective British study has found that Indian Asians with acute coronary syndrome presenting to a chest pain clinic were, on average, almost 10 years younger than white Europeans presenting for the same reason, and they also had a much higher incidence of triple-vessel disease not explained by conventional risk factors.
Dr Anoop Mansoor (Imperial College, London, UK) presented the results in a poster at the recent
European Society of Cardiology Congress 2008.
Mansoor told heartwire the findings indicate that large-scale screening of Indian Asians is needed "from a young age, so that we can stop premature disease." Currently, UK recommendations stipulate that screening should begin in the general population from the age of 40 onward, he says, so he believes that Indian Asians should be screened from the age of 30. "Even though the average age of Indian Asian patients we saw was 60, the disease starts much younger, and we have even seen a number of patients in their 20s who come in with severe coronary artery disease," he said.
Such people should be screened for all conventional risk factors, particularly diabetes, which is especially prevalent in this population, he noted, and they should be given treatment where necessary and advice on lifestyle modifications.
More triple-vessel disease in South Asians is "perplexing"
We have even seen a number of [Indian Asian] patients in their 20s who come in with severe coronary artery disease.
Mansoor said his team decided to conduct the study because the reasons underlying the twofold higher CAD mortality in Indian Asians compared with European whites is not known. Also, "there were no recent studies in an Indian Asian population with modern treatment anywhere in the literature, so we decided to take a prospective look and compare Indian Asians with whites as they came in to a day-to-day clinical practice."
They followed 584 patients with ACS admitted to a chest pain clinic at Ealing hospital in west London from May 2005 to July 2007, comprising 327 patients of Indian Asian origin (from the Indian subcontinent—India, Pakistan, and Bangladesh—or Sri Lanka) and 257 white Europeans. Over 60% of patients of both ethnic backgrounds were male.
The Indians were, on average, 63 years of age compared with 70.7 years for the whites (p<0.001).
They also had significantly increased prevalence of diabetes (odds ratio 3.4, p<0.001), dyslipidemia (OR 1.8, p=0.01), hypertension (OR 1.7, p=0.05), and history of CAD (OR 1.7, p=0.01) compared with European whites, adjusted for age and sex. Indian Asian patients had much lower smoking rates than the whites, however (OR 0.14, p<0.001).
And triple-vessel disease was more common in the Indian Asians than in the whites (17% vs 11%; p=0.009), and in regression analysis this was not accounted for by the higher prevalence of conventional cardiovascular risk factors in Indian Asians (p=0.02), a finding Mansoor said was "quite perplexing."
There were no differences in hospital use of coronary angiography, PCI, and CABG between the two populations.
"Indian Asians with ACS present almost 10 years earlier and have more extensive angiographic CAD than European whites," Mansoor concluded, adding that the reasons underlying this remain to be identified. "Large-scale prospective data comparing outcomes of ACS in Indian Asians and European whites are urgently required."
Public information campaign needed
In the meantime, Mansoor said a public information campaign directed at young Indian Asians is needed. This is particularly true of young men who are "not overweight—to the contrary, they have quite active lifestyles so they do not see themselves as at risk."
The pattern of ACS seen in Indian Asian women was similar to that seen in whites, he noted; that is, they presented on average 10 years later than Indian Asian men, but this was still 10 years earlier than white women.
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September 19, 2008 06:10 (EDT)
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asian indians early acs
Sad commentary on failure of primary prevention in this population group, not just in Europe.
Traditional ldl based goals for this population come up woefully short. Visceral adiposity is often not recognized in this population. Combination lipid therapy including niacin is usually needed, but rarely given. |
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September 20, 2008 12:39 (EDT)
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Indian Asians with ACS
Astonishingly the author is unaware of" recent studies in an Indian Asian population with modern treatment anywhere in the literature"..... because I am certain that 'the heart.org' has extensively reported recent studies on Indians with ACS.
A large study involving 20,000 Indian patients with ACS (Xavier D,Pais P, Devereaux PJ,et al. 'Create Registry'.Lancet 2008:371:1435-42.) described in fairly great detail the risk factors in these patients and their treatment regimens in as many as 89 centers in 50 cities in India.
Moreover risk factors for early myocardial infarction in South Asians have also been published ( JAMA 2007;297:286-294) with the conclusions that risk factors in South Asians are comparable to those seen in non- Asians ,albeit appearing slightly earlier.....and that South Asians most probably do not harbor any exotic or mysterious risk factors for coronary artery disease.
Certainly more studies are needed to better understand coronary artery disease in Indian Asians ( there is a huge population group out there!!).... but certainly not with the "perplexed" mindset that Indian Asians are somehow genetically significantly different from the rest of their neighbors on this planet.
More importantly researchers must appreciate that the Asian Indian growing up in their own country would constitute an entirely different cohort for studies than their cousins adapting to the plush but emotionally altered environment of the West.
I have always had this sneaking suspicion( I could be wrong of course) that South Asians where ever they may be...... are more inclined to sit back and watch TV or melt into their computers for hours together.... than manufacture a few smelly drops of their own perspiration.
This is THE RISK FACTOR that merits ( besides other) immediate intervention on a war footing. |
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September 20, 2008 06:34 (EDT)
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Clarification:
Deepak,
I believe Dr. Mansoor was referring to necessity of organizing a study of Indian Asians who had migrated to England or other countries. Much like the concerns for the Japanese who fair better than Americans while living in their country but develope increased rates of CAD when they come to America, it deserves a look. Even Japanese women who have relatively comfortable menopause develope hot flashes when they come to America.
For the record, some of our own beloved friends and acquaintainces who are East Indian have developed diffuse disease without the aid of a cigarette after coming to the US, which is very unusual for their age adjusted young American counterparts.
So, something's up with all of this and it deserves a look.
Melissa |
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September 29, 2008 01:18 (EDT)
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Much of this needed data,... is already out there,..
"Traditional" CV risk factors have probably the least clinical utility in this population. The "Devil" is in the details: Insulin Resistance, low HDL2[b], pattern "B", Lp(a)
2 or more of these are found @ THE HIGHEST PREVELANCE VS. ANY OTHER ETHNIC GROUP. Reference Enas Enas, MD. Agree 100% w S. Tatar. |
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October 1, 2008 09:03 (EDT)
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agree
CJ,
I agree. A very nice East Indian gentleman has established disease and on statin, total cholesterol, HDL, LDL and TG's were all NORMAL. He then went to the local primary prevention clinic (which we fully support but have no financial ties with) and was astounded that despite his normal weight, his insulin level was WAY up. So, he's a skinny diabetic, now on niacin and watching his carbs.
Melissa |
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October 1, 2008 10:07 (EDT)
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For difficult to titrate niacin patients,..
CarlsonLabs.com
They have a 100 count, 50 mg,.. about $3 / bottle. Especially useful if they can`t take/tolerate an NSAID [325 ASA for examp] to "bridge" past the 'tachyphylactic' flush.
50 mg TID, ease up as patient gains confidence. My wife flushed horribly on 500 mg ER-niacin,.. but, she can`t take ASA. Took Carlson`s for 90 days,.. SLOOOW, 1-50 mg / meal, at first,.. up to 6 - 50 mg / meal. Went back to the 500 mg ER-niacin after that, ~90 days,.. NO FLUSH AT ALL !!! She now takes 2000mg / day. Nice option for the coumadin patient as well, so as not to "need" the ASA. Luteolin not yet ready for "prime-time".
Old "Castelli" standby is still best for those who can start @ 500 mg &/or tolerate ASA:
The "Alka-Sauce" protocol: 1 or 2 - 325 mg Alka-Seltzer tabs [Varveris in Naples, FL often uses 2, sometimes w small dose Benadryl for 1st week] in SMALL amount of H2O; swallow 3 TBS applesauce [any small high-fiber snack]; 'lastly' wash down 500 mg ER-niacin with Alka-Seltzer [Wal-Mart no-name sometimes works better, really can`t say why]. Sounds involved, but most folks tachy down & no longer need preventative measures [anti-flush maneuvers] after 60-90 days. This is distilled down from 20-30 individuals over 30-40 years, I believe Castelli was "1st" on the Alka-Seltzer idea: This ensures they do NOT forget the ASA,... you wash the 'dry' pill / niacin down with the ASA. the compliance with the ASA/NSAID is what your after !! Try this on patients for your next 90 days of niacin 'starts',.. it will convert you. Kinda neat, really,.. ;-) |
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October 1, 2008 11:33 (EDT)
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Lp(a) prevalent in Indian population with CAD/MetSyn
What treats Lp(a) effectively?
--carb restriction (no grains, no legumes -- which of course is the typical Indian diet -- roti, dal, lentils, etc) -- CR shuts off IR and turns on PPARs
--strength train/moderate intensity exercise
--fish oil -- not much seafood in modern Indian cuisine
--krill oil (via RXR RAR activation)
--saturated fats (via PPAR-delta gamma alpha activation) -- yes 6 eggs/day and cholesterol (!!) reduces sdLDL and raises HDL2b dramatically (and reduces toxic, plaque/cancer causing HDL3c)
--of course niacin (Slo-niacin, NIASPAN)
Fish oil is easy and ideal -- freezing it reduces burps/GI upset/ heartburn. For 8.5 grams daily EPA + DHA requires a lot -- NOW SUPER EPA is cheap and no Hg.
25% Lp(a) reduction:
Hermann W et al. Med Klin (Munich). 1989 Sep 15;84(9):429-33. [Modification of the atherogenic risk factor Lp(a) by supplementary fish oil administration in patients with moderate physical training][Article in German]
14% Lp(a) reduction (24% reduction in Responders):
Hermann W. Am J Cardiol. 1995 Sep 1;76(7):459-62. Comparison of effects of N-3 to N-6 fatty acids on serum level of lipoprotein(a) in patients with coronary artery disease.
-BG |
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October 1, 2008 11:57 (EDT)
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Roger that BG,...
One of the thought leaders in ENDO, who`s name escapes me now, [Canadian, lots of data on Inuit CAD] influenced us to use 6-9 "normal" 1gm caps of fish oil combo w 1-2 gms of niacin. Best of both worlds. Dramatic TG, VLDL3 reductions,
Lp(a), pattern B convesion with very robust HDL2[b], that seems to plateau only after 2-3 years. The niacin 'stabilizes' the LDL rise with the omegas,.. niacin amplifies the good TG/VLDL3 drop without the large # of FO capsules. Shhoting blind-folded, 10 mg simva, 6 gms 'common' FO & 1-2 gms ER or IR niacin,.... that pretty much covers it. With IR rampant in the populace,.. 2 hr PPG > 140,.. how should we determine who to screen ? They do NOT always present with elevated TG`s or central adiposity. Without HDL2[b] plus pattern B measurement, many go un-noticed until they are already DM. The % who would likely fail the PPG > 140 in high-school now, with the juvenile obesity epidemic, frightens me. In 10 years the rate of DM over the age of 25 will be double. When do you treat this ? After their fasting gluc is > 126 ? If they don`t reduce carbs, exercise & lose weight we can`t just shake our heads,... It reminds me of the recent controversy of statin use in pediatrics. |
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October 2, 2008 12:00 (EDT)
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OH !! By the way BG,..
NKO has competition now. The original harvester of krill,.. Aker Biomarine. Jedwards will distro in the US. Price may drop, and a 2nd competitor may increase the customer service and quality. |
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October 2, 2008 09:59 (EDT)
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Can we put simva 10/d, FO, B3 in the global H2O?
If I had cash I'd buy Jedwards...*ha*
NKO aint bad but the price sucks MEGA RED (from NKO of course) $18/mon from Costco...so...competition is GOOD. Krill is like petrol/Opec -- just one distro and that aint good. (like stents/cabgs right?) Maybe I should go into Krill instead of CAD prim/sec prevention (more profitable!) -- Chinese eat a 'bbq sauce/satay' rich in Krill all smashed up. You'd like! (pour off the toxic omega-6 soybean oil)
Taurine -- raises HDL (presumably HDL2b too --see end). Esp synergistically with FO. Like life -- synergism RULES.
Do you have data on Krill and Lp(a) -- can't locate that???!!! would like ur help. THANX in advance.
btw... I'm into Smack and Mack ('SM' right?)
I read the Castelli interview -- very enlightening -- awesome MAN/mensch. Not many exist anymore. And he beat his family curse -- ie CAD. That's fantastic. So generous with knowledge. We all gotta monkey don't we?
Yamori Y.
Food factors for atherosclerosis prevention: Asian perspective derived from analyses of worldwide dietary biomarkers.
Exp Clin Cardol. 2006 Summer;11(2):94-8. PMID: 18651042
Elvevoll EO, et al.
Seafood diets: Hypolipidemic and antiatherogenic effects of taurine and n-3 fatty acids.
Atherosclerosis. 2008 Jan 31. PMID: 18242615
Dirican M, Taş S, Sarandöl E.
High-dose taurine supplementation increases serum paraoxonase and arylesterase activities in experimental hypothyroidism.
Clin Exp Pharmacol Physiol. 2007 Sep;34(9):833-7. PMID: 17645625
-G |
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October 3, 2008 04:12 (EDT)
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a question for you fish oil braniacs
Though I don't think I have any Inuit blood: Just curious about your opinion on Carlson Lab's Very Finest Fish oil, which I still prescribe. It's great for those who can't swallow a pill the size of their shoe and it's easy to slip it into any food. It's about 27 dollars for 2-3 months supply (depending of course on how much you actually take). Downside: large glass brown bottle, but it will recycle in some places I suppose. Tastes yummy, no joke, lightly lemon flavored.
Melissa |
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October 5, 2008 11:48 (EDT)
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Pharmaomega -- baby-sized FO caps $$$$
Hi Melissa -- I've tried various brands and I love the taste of Carlson's too! Some friends say it reminds them of Lemon-Pledge though. We may all be part-Inuit now w/all the FO we take. And growing gills! Here are some other brands that are excellent -- small caps are available for children or people who may have difficulty swallowing (and don't like liquid) -- scroll to end of post.
drbganimalpharm.blogspot.com/2008/08/olympic-global-domination-and-all.html
The trad'l Indian diet actually maybe one of the most cardioprotective (outside of Inuit). The conversion to Western diets is quite worrisome w/exponential increases in obesity MetSyn and CAD. Is the Lp(a) incidence genetically more prevalent in the Indo-Asian pop?? The MetSyn CAD patients I've seen are very young -- all have Lp(a). And even if T2DM-free, microalbumunuria++ significantly existing. If they do have T2DM, then retino- nephro- and peripheral neuropathies are all devastingly present.
Except for the exceedingly high carb-intake (wheat/lentils), the trad'l Indian diet is in fact very cardio-protective:
--chai -- tea and spice bioflavonoids
--fenugreek -- many soak seeds overnight and eat in the morning --lowers insulin, glucoses, VLDL, TG, HDL3c (presumably), raises HDL2b, sdLDL
--ghee -- butyric &lauric acids and other agonists of PPAR-d -a -g (see below)
--tumeric
--cucurmin -- one of the earth's strongest antioxidants
--small and large fishes consumption
--gamey goat meat and milk -- high EPA DHA CLA
Haeri MR et al The effect of fenugreek 4-hydroxyisoleucine on liver function biomarkers and glucose in diabetic and fructose-fed rats.
Phytother Res. 2008 Aug 4
Krishnaswamy K Traditional Indian spices and their health significance. Asia Pac J Clin Nutr. 2008;17 Suppl 1:265-8.
Gupta A et al Effect of Trigonella foenum-graecum (fenugreek) seeds on glycaemic control and insulin resistance in type 2 DM: a double blind placebo controlled study. J Assoc Physicians India. 2001 Nov;49:1057-61.
Curcumin increases HDL 29% in healthy volunteers
Soni KB Effect of oral curcumin administration on serum peroxides and cholesterol levels in human volunteers. Indian J Physiol Pharmacol. 1992 Oct;36(4):273-5.
High-carb Western diet is powerfully atherogenic (v. high fat) -- classic!!
Williams PT, Dreon DM, Krauss RM. Effects of dietary fat on high-density-lipoprotein subclasses are influenced by both apolipoprotein E isoforms and low-density-lipoprotein subclass patterns. Am J Clin Nutr. 1995 Jun;61(6):1234-40. PMID: 7762523
Lauric acid -- found in ghee/butter/coconut oil -- raises HDL2b
Lagrost L et al Variations in serum cholesteryl ester transfer and phospholipid transfer activities in healthy women and men consuming diets enriched in lauric, palmitic or oleic acids. Atherosclerosis. 1999 Feb;142(2):395-402. |
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