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References

1 Roerecke M, Rehm J. The cardioprotective association of average alcohol consumption and ischemic heart disease: a systematic review and meta-analysis.Addiction 2012; 107: 1246-1260.

2 Holmes MV, Dale CE, Zuccolo L, et al. Association between alcohol and cardiovascular disease: Mendelian randomization analysis based on individual participant data. BMJ 2014; 349: g4164.

3 Ronksley PE, Brien SE, Turner BJ, Mukamal KJ, Ghali WA. Association of alcohol consumption with selected cardiovascular disease outcomes: a systematicreview and meta-analysis. BMJ 2011; 342: d671.

4 Chikritzhs T, Stockwell T, Naimi T, Andreasson S, Dangardt F, Liang W. Has the leaning tower of presumed health benefits from ‘moderate’ alcohol use finally collapsed? Addiction 2015; 110: 726-727.

5 Leong DP, Smyth A, Teo KK, et al. Patterns of alcohol consumption and myocardial infarction risk: observations from 52 countries in the INTERHEART case-control study. Circulation 2014; 130: 390-398.

6 Whitman IR, Agarwal V, Nah G, et al. Alcohol abuse and cardiac disease. J Am Coll Cardiol January 2017; 69:13–24.7 Kodama S, Saito K, Tanaka S, et al. Alcohol consumption and risk of atrial fibrillation: a metaanalysis. J Am Coll Cardiol 2011; 57: 427–436.8 Criqui M. H., Thomas I. C. Alcohol Consumption and Cardiac Disease Where Are We Now? J Am Coll Cardiol January 2017; 69: 25-27.9 Wright J.T. Jr., Williamson J.D.,Whelton P.K.,et al. (2015) A randomized trial of intensive versus standard blood-pressure control. N Engl J Med

November 26 2016; 373: 2103–2116.10 Bangalore S., Messerli F.H., Wun C.C., et al. (2010) J-curve revisited: an analysis of blood pressure and cardiovascular events in the Treating to New

Targets (TNT) Trial. Eur Heart J September 2010; 31: 2897–2908.11 Bhatt D.L.,James G.D., Pickering T.G.,Devereux R.B. (1996) Relation of arterial pressure level and variability to left ventricular geometry in normotensive

and hypertensive adults. Blood Press Monit 1: 415–424.12 Cooper-DeHoff R.M., Gong Y., Handberg E.M., et al. (2010) Tight blood pressure control and cardiovascular outcomes among hypertensive patients

with diabetes and coronary artery disease. JAMA 2010; 304: 61–68.13 McEvoy J.W., Chen Y., Rawlings A., et al. (2016) Diastolic blood pressure, subclinical myocardial damage, and cardiac events: Implications for

blood pressure control. J Am Coll Cardiol October 2016 68: 1713–1722.

HEARTBEATA Publication of South Jersey Heart Group

January 2017

The end of a year is a time to reevaluate, resolve, and

begin anew. In this Heartbeat, I want to share some news

I’m not happy about, which has led to my New Year’s

resolution for 2017.

Investigators are calling into question the long-held

notion that “moderate” alcohol consumption offers health

benefits, especially cardiovascular disease (CVD) benefits.

They’re saying there may be some positive effects, but they

exist at lower, not daily, “doses” of ethanol, and may even

be nonexistent.

This is “hard to swallow” news, considering all the

positive press in recent years given to the beneficial effects

of moderate alcohol consumption. I’m a firm believer in

two drinks/day as per our August 2016 Heartbeat on diet

(maybe a touch over).

J Curve

There is a relationship between mortality from CVD and

the average amount of alcohol consumed per day that is

consistent with a J-shaped curve. A similar relationship

has been reported for mortality from ischemic heart disease

(IHD) in one meta-analysis. Compared to long-term

abstinence, daily consumption of small or moderate

amounts of alcohol was associated with reduced mortality

from IHD, with the nadir of the relative risk curve at about

31 g of ethanol per day for men and a substantially lower

amount for women (about 11 g/day for IHD mortality—

less than one drink/day —and 14 g/day for IHD morbidity).1

(See graphic below) At higher daily intakes of alcohol, the

risk reduction was gradually replaced by increased risk.

Lower recommendations for women is not misogynist,

but based on the fact that alcohol metabolism in the liver

is slower for women.

Sweet Spot

The sweet spot (lowest point of the J), where we always

want to go (most benefit with the lowest risk) is moving

left and seems smaller before the risk goes up.

The positive press in recent years given to the beneficial

effects of moderate alcohol consumption is based on

many observational studies without statistical support.

The problem is the fact that bad news on the topic just

doesn’t seem as likely to hit the headlines. There is

Alcohol and the Heart

certainly a large audience for “good news” about alcohol

consumption. Any possibility of benefit is welcome news

to those who enjoy its consumption (me) and to those

who profit from its sale.

Data from new methodologies, such as Mendelian

randomization and data from large international

meta-analysis studies, have led us to rethink this

J-shaped relationship in that the dose-response has

shifted to the left. In one Mendelian analysis of 261,991

individuals of European descent, reduction of alcohol

consumption, even for light-to-moderate drinkers (one

drink/day for women and two drinks/day for men),

was beneficial for cardiovascular health. 2

There are a large number of individual variables that can

influence response to alcohol, including genetics, sex,

race/ethnicity and socioeconomic status. 3 In recent years,

there has been growing concern regarding whether

purported beneficial effects of moderate alcohol use are

real or are attributable to confounding factors not

adjusted for in the studies performed. 4 People who drink

one to two drinks per day usually have better health habits.

New information, in an analysis of data from 52

countries—the INTERHEART study—have “moved the

J curve” left. In men and women, alcohol consumption

exceeding one to two drinks/day is associated with an

increase in the relative risk of hypertension. Binge

drinking on a regular basis is likely to “acutely” increase

blood pressure and the risk of stroke. Binge drinking,

defined as six or more drinks in a single episode of

drinking, significantly increases the risk of myocardial

infarction (MI) over the next 24 hours (odds ratio: 1.4;

p < 0.01) compared to less consumption of alcohol. 5

This risk is even worse for people greater than 65 years old.

The protective association between alcohol use and

MI was no longer significant when any alcoholwas

consumed more than four times a week—so much for

the protective effects of a drink a day. “Alcohol use”

with a frequency of one to four times a week

(again, not a day — a week) was associated with

a reduced risk of MI; anything more than that

had a deleterious effect on risk of MI.

Importantly, the INTERHEART investigators noted that

the protective effect was not uniform among all regions

or populations. Where there seemed to be a protective

effect in Europe, North America and Australia/New

Zealand, there was none at all seen for people in

Southeast Asia. Also, the protective association of alcohol

against MI was greater in women and in people ≥ 45years of age.

Stroke is also an important consideration. Evidence

suggests that the level of alcohol consumption reported

to be protective for the heart is lost for the brain in terms

of incident stroke and stroke mortality. In other words,

levels of consumption, which seem protective for the

heart, actually increase risk of stroke.

No Sweet Spot

The risk of atrial fibrillation begins at the lowest doses

of alcohol consumption and increases in a dose-

response fashion.6, 7

An editorial comment in this month’s JACC concludes,

“Alcohol is a potentially addictive and dangerous drug,

both for the cardiovascular system and multiple other

organ systems. The recent infatuation with the potential

benefits of light-to-moderate drinking for CVD

protection appears to be based on observational and

subtly confounded data, rather than on randomized

clinical trial evidence, and perhaps on more than a little

wishful thinking.” 8

Where are we now?

• A low-to-moderate level of alcohol consumption (one to two drinks/day, but not every day) is probably not harmful to overall cardiovascular health—one for the ladies and two for the gentlemen—skipping at least three/day/week. This will be the hard part, which I feel is the “new safer moderate sweet spot.”

• In the absence of randomized controlled clinical trials, healthcare professionals should not recommend alcoholconsumption as a primary or secondary lifestyle intervention to decrease risk, but rather should continue to recommend established strategies, such as physical activity and a healthy diet as per our July and August 2016 Heartbeats (on our website—www.SJHG.org.)

• Lower levels may be appropriate for specific groups—such as the elderly or particular racial groups (e.g., in South Asia and the Middle East, and African Americans).

• Those who currently abstain from alcohol should not begin drinking to reduce their risk of health problems.

Diastolic Blood Pressure: What’s Optimal?

Since we now all can relate to the J curve, I thought it

would be good to apply it to another topic. For years, there

has been a debate about not treating blood pressure (BP)

too vigorously for fear of decreasing diastolic pressure

too much.

Randomized data regarding the optimal BP target conflict,

with the most recent data from SPRINT (Systolic Blood

Pressure Intervention Trial) suggesting that lower is

indeed better.9 Intuitively, though, it would seem that

there should be a lower limit below which BP reduction

would be harmful—the so-called J-curve.10 Coronary

blood flow occurs predominantly during diastole; as such,

a reduction in diastolic BP (DBP) would be expected to

decrease coronary blood flow, especially if obstructive

coronary artery disease (CAD) is present. Hypertension

that results in left ventricular hypertrophy may further

increase myocardial demand, but overly aggressive

hypertension therapy may decrease coronary perfusion

pressure, creating a supply/demand mismatch.11 Several

observational analyses support the existence of a J-curve.12

An important study by McEvoy et al. presents an

insightful analysis of 11,565 subjects from the ARIC

(Atherosclerosis Risk in Communities) cohort.13

Investigating the association between high-sensitivity

cardiac troponin-T (hs-cTnT) levels and DBP, they found

that compared with people with DBP of 80 to 89 mm

Hg, those with a DBP of 60 to 69 mm Hg had higher

prevalence of baseline hs-cTnT ≥14 ng/l. Those with DBP <60 mm Hg had an even higher prevalence.

The hypothesis suggested by these associations is that

low DBP causes ongoing subclinical myocardial

Guest Editor: Peter Bulik, DO

Cardiology Fellow, PGY V, Rowan SOM

Mario L Maiese, DO, FACC, FACOI

Clinical Associate Professor of Medicine, Rowan SOM

Email: maiese1@comcast.net

Sign up to receive Heartbeat online: www.sjhg.org

Heartbeat is a South Jersey Heart Group publication.

damage that leads to chronic troponin elevation,

explaining an association between low DBP and

adverse cardiac outcomes.

Compared with a DBP of 80 to 89 mm Hg, a DBP <60

mm Hg was significantly associated with incident CAD

and mortality. Importantly, there was not an association

with stroke. The association between DBP and incident

CAD was strongest when the baseline level of hs-cTnT

was ≥14 ng/l (interaction p < 0.001), suggesting that troponin elevation may not only have been a marker

of myocardial damage, but also on the causal pathway

for coronary events. These associations were most

pronounced among patients with baseline systolic blood

pressure (SBP) ≥120 mm Hg, which meant that thosewith an elevated pulse pressure (PP = SBP -DBP) >60

mm Hg were at particular risk.

Conclusion

Particularly among adults with a SBP ≥120 mm Hg, andthus elevated PP, low DBP was associated with subclinical

myocardial damage and CHD events. When titrating

treatment to SBP <140 mm Hg, try to ensure that

DBP levels do not fall below 70 mm Hg, and

particularly not below 60 mm Hg.

We at Lourdes Cardiology

Services wish you all a very

happy and healthy new year.