effect of cigar smoking on the risk of cardiovascular...

JOURNAL OF INSURANCE MEDICINECopyright © 2000 Journal of Insurance MedicineJ Insur Med 2000;32:42-45

LITERATURE REVIEW

Effect of Cigar Smoking on the Risk ofCardiovascular Disease, Chronic ObstructivePulmonary Disease, and Cancer in Men

Keith Clark

Reference: Iribarren C, Tekawa IS, Sidney S, Friedman GD. Effect ofcigar smoking on the risk of cardiovascular disease, chronic obstruc-tive pulmonary disease, and cancer in men. N Engl J Med. 1999;340:1773-80.

Address: Western & Southern LifeInsurance Company, 400 Broadway,Cincinnati, OH 45202-3341.

Correspondent: Keith T. Clark, MD,Vice President & Medical Director,Western-Southern Life InsuranceCompany.

Key words: Smoking, cigar, tobac-co, morbidity, males, cardiovascularheart disease, chronic obstructivepulmonary disease, cancer.

Received: August 25, 1999.

Accepted: December 1, 1999.

C igar consumption has been increasing inthe United States since 1993. There are

several likely reasons for this increase, includ-ing promotion by the mass media and the be-lief that cigar smoking is generally thought tobe safer than cigarette smoking. The associ-ation of cigar smoking with cancer of the or-opharynx and the upper aerodigestive tractand chronic obstructive pulmonary disease(COPD) has been well documented by a num-ber of studies. However, the association of ci-gar smoking with cardiovascular heart dis-ease (CHD) has not been determined defini-tively.

This article reported a retrospective studythat evaluated the association of cigar smok-ing with several disorders. Although thestudy has some limitations that are common

with retrospective studies, it is well thoughtout and well designed. It offers substantialevidence that cigar smoking is associatedwith an increased risk of COPD and relatedconditions and CHD and that cigar smokingis associated with an increased risk of cancerof the oropharynx and lung cancer. It also of-fers support for an apparent dose-response(number of cigars smoked daily) associationwith multiple disorders.

The study cohort was a subpopulation of17,774 men aged 30 to 85 years enrolled inthe Kaiser Permanente Medical Care Programof Northern California. They were selectedfrom a larger population of 207,165 members(46% male, 54% female) aged 14 and up thathad had voluntary health examinations at thetime of their enrollment from 1964 through

42

CLARK-~CIGAR SMOKING IN MEN

Table 1. Incidence and Risk of Cardiovascular Heart Disease and Chronic Obstructive Pulmonary Disease inRelation to Cigar Smoking

Relative Risk for Cigar Smokers vsOutcome Non-Cigar Smokers, Age-Adjusted (95% CI)* P Value

Coronary heart diseaseIschemic strokeHemorrhagic strokePeripheral artery diseaseChronic obstructive pulmonary disease and related

conditions

1.27 (1.12-1.45) <.00011.07 (0.85-1.34) .551.12 (0.67-1.90) .651.29 (0.84-1.98) .231.45 (1.10-1.91) .008

* CI indicates confidence interval.

1973. Entry was limited to men who reportednever smoking cigarettes and were not pipesmokers at the time they entered the study.Women were not studied because of an in-adequate number of entrants (only 25 report-ed smoking cigars and not cigarettes or apipe). Of the 17,774 entrants, 8.7% (1546) cur-rently smoked cigars; 91.3% (16,228) did notcurrently smoke cigars and were used for thecontrol population.

Cigar smokers were stratified by daily con-sumption: <5 cigars daily, 5-10 cigars daily,and >10 cigars daily. No information wasavailable about the length of time dgars hadbeen smoked, the degree of inhalation, or thetype of cigar usually smoked. No history ofcigar or pipe smoking was asked, so formercigar and pipe smokers would have been inboth groups (cigar smokers and the controlpopulation).

If more than one health check-up was avail-able, the first one was used. Several baselinemeasurements were taken: (1) serum choles-terol; (2) self-reported alcohol use stratifiedby daily consumption: none, 1-2 drinks daily,3-5 drinks daily, and 6 or more drinks daily;and (3) presence or absence of diabetes mel-litus, cardiovascular disease, or COPD basedon patient history.

Follow-up for the development of cancerwas done using hospitalization records andtumor registries. COPD and CHD follow-upwas done using hospital discharge files. Hab-its followed up included the continuation ofcigar smoking and switching to or the addi-

tion of cigarette smoking. Age-adjusted rateswere used in the statistical analyses. Multi-variate analysis of cancer and COPD includedthe following covariates: age, race, body massindex, history of diabetes mellitus, current al-cohol consumption (stratified), and any re-cent or past occupational exposure (to air-borne pollutants). The multivariate analysisof cardiovascular disease also included thefollowing covariates: education (no college vsany college), systolic blood pressure, and to-tal serum cholesterol.

RESULTS

Person-years of follow-up were 228,512 fornon-cigar smokers and 20,176 for cigar smok-ers. Cigar smokers were more likely to haveno college education and had significantlyhigher alcohol consumption. By history, of17,774 entrants, 485 had CHD only, 657 hadCOPD only, 53 had CHD and COPD and16,579 reported neither CVD nor COPD. Of1546 cigar smokers, 76% (1177) smoked <5cigars daily, 17% (263) smoked 5 or more dai-ly, and for 7% (106), the number smoked dai-ly was unknown.

The relative risk using age-adjusted rate ofoccurrence per 10,000 person years was high-er for cigar smokers (relative to the controlgroup) for COPD and related conditions andfor CHD (Table 1). There was no associationwith ischemic or hemorrhagic stroke or pe-ripheral artery disease.

Cigar smokers had an increased risk for

43

JOURNAL OF INSURANCE MEDICINE

Table 2. Incidence and Risk of Cancer in Relation to Cigar Smoking

Relative Risk for Cigar Smokers vsOutcome Non-Cigar Smokers, Age-Adjusted (95% CI)* P Value

Cancer of the oropharynxCancer of the upper aerodigestive tractLung cancerPancreatic cancerCancer of the kidneyBladder cancerAll smoking-related cancersColorectal cancerAll cancer (except nonmelanoma skin cancer)

2.61 (1.18-5.76) .022.02 (1.01-4.06) .042.14(1.12-4.11) .021.21(0.51-2.88) .661.08(0.43-2.71) .871.05, (0.55-2.01) .891.42 (1.02-1.98) .041.12 (0.80-1.57) .511.07 (0.93-1.25) .35


Table 3. Multivariate-Adjusted Risk of Cardiovascular Heart Disease, Chronic Obstructive Pulmonary Disease, andCancer in Relation to the Amount of Cigar Smoking

<5 Cigars per Day 5 or More Cigars per Day

Relative Risk Relative RiskOutcome (95% CI)* P Value (95% CI)* P Value

Coronary heart disease 1.20Ischemic stroke 1.02Peripheral artery disease 1.09Chronic obstructive pulmonary disease and related1.30

conditionsOropharyngeal cancer 1.34Cancers of the upper aerodigestive tract 1.12Lung cancer 1.57All smoking-related cancers 1.17All cancers (except nonmelanoma skin cancer) 1.11

(1.03-1.40) .02 1.56(1.21-2.01) <.001(0.78-1.34) .88 1.29(0.85-1.94) .23(0.64-1.86) .73 2.17(1.09-4.32) .02(0.93-1.81) .12 2.25(1.39-3.65) .001

(0.41-4.42) .63 7.20 (2.44-21.2) <.001(0.40-3.12) .84 5.20 (2.00-13.5) <.001(0.67-3.66) .30 3.24 (1.01-10.4) .04(0.77-1.77) .46 2.26 (1.26-4.07) .01(0.94-1.31) .22 0.98 (0.69-1.38) .89


cancer of the oropharynx, upper aerodiges-tive tract, or lung (Table 2). The relative riskfor all smoking-related cancers was only mar-ginally significant (note that the lower 95%confidence interval is only 1.02). There wasno significant difference of the other cancersstudied or all cancers combined.

Cigar smokers were stratified into <5 ci-gars daily and ->5 cigars daily to determineif there is a dose-response relationship (Table3). For the ->5 cigars group, the risk of CHD,COPD, and cancer of the lung and upperaerodigestive tract was statistically signifi-cant, whereas it was not (statistically signifi-cant) for those that smoke <5 cigars daily.

The same was observed for all smoking-re-lated cancers but not for all cancers com-bined. There was a marginally increased riskof peripheral arterial disease for patients whosmoked 5 or more cigars daily.

As compared to studies of cigarette smok-ing, the relative risks for COPD and lung can-cer were less for cigar smokers. However, theauthors pointed out a confounding factor thatunderestimates the risk of cigar smoking inthis study. Smoking habits for the cohort aredetermined at the beginning of the studywith incomplete follow-up. At 4-year and 8-year rechecks, where 28% (438) and 11% (171)of the cigar-smoking cohort reported, respec-

CLARK--CIGAR SMOKING IN MEN

tively, 64% (281) and 50% (86), respectively,reported that they still smoked cigars. Incom-plete follow-up would tend to overestimatethe exposure (since not every cigar smokerpersisted in smoking cigars) and as a result,underestimate the risk.

Additionally, in this study, cigar smokers

have significantly higher alcohol consump-tion than the control population. The higheralcohol use in cigar smokers is a confoundingfactor because alcohol has been associatedwith an increased risk for oropharyngeal can-cer and the upper aerodigestive tract in cig-arette smokers.

45


LITERATURE REVIEW

Palindromic Rheumatism and the Risk forRheumatoid ArthritisWayne Heidenreich, MD

Reference: Gonzalez-Lopez L, Gamez-Nava J, Gian J, et al. Prognos-tic factors for the development of rheumatoid arthritis and otherconnective tissue diseases in patients with palindromic rheumatism.J Rheumatol. 1999;26:540-545.

Address: Northwestern Mutual Life,720 E Wisconsin, E14B, Milwaukee,WI 53202-4797.

Correspondent: Wayne Heidenreich,MD, Medical Director.

Key Words: Rheumatoid arthritis,rheumatoid factor, palindromicrheumatism, prognosis.

Received: December 1, 1999.


p~ alindromic rheumatism can evolve into

rheumatoid arthritis (RA) or connectivetissue disease (CTD). It is defined as the pres-ence of episodic attacks of joint pain accom-panied by signs of joint inflammation withcomplete remission between episodes. It canaffect a single joint or many joints; it may lasthours to days; and it may recur with a fre-quency of weeks to months.

This study was based upon a cohort withthe diagnosis of palindromic rheumatism re-ferred to rheumatologists at the University ofAlberta. This cohort was followed to assessthe prognostic factors for the development ofRA or CTD.

STUDY METHODOLOGY

This was a retrospective study of a popu-lation of 127 people who met documented in-clusion criteria for the diagnosis of palindro-mic rheumatism. They were identified fromover 4900 referrals to the University of Al-berta for arthritis. The criteria included nor-mal radiographs and the exclusion of other

recurrent monoarthritedes such as gout andchondrocalcinosis. This cohort was studiedbetween 1986 and 1996.

Variables of interest included the numberand identity of joints involved, frequency ofattacks, duration of attacks, and presence ofrheumatoid factor. The duration of palindro-mic rheumatism was estimated from the timeof initial attack until the development of RAor CTD or until the last consultation if thepatient did not evolve another systemic rheu-matologic disease.

Differences in this "survival time" (free ofRA or CTD other than palindromic rheuma-tism) were evaluated using Kaplan-Meiermethods. Cox proportional hazard modelswere used to identify variables associatedwith the development of RA or other CTD.Both univariate and multivariate Cox regres-sion analyses were performed.

RESULTS

Women comprised 65% of the 127 subjects.The mean age at onset of attacks was 40

46

HEIDENREICH--PALINDROMIC RHEUMATISM

years. The mean duration of symptoms was6 years. The most commonly involved jointswere: wrist (65% of patients), knee (60%), me-tacarpophalangeal (56%), and shoulder(35%). The rheumatoid factor (RF) was posi-tive in 39% of patients. Forty-three (34%) ofthe study group developed rheumatoid ar-thritis or a connective tissue disease duringthe period of observation.

A comparison of the clinical findings foundin those who developed RA or CTD withthose who did not revealed no significant dif-ference in mean age at onset (ages 42 and 38,respectively), sex, number of attacks (18 and13), length of attacks (4 days), or frequencyof knee involvement. There was a statisticallysignificant association between involvementof the wrist, proximal interphalangeal joints(PIP), and metacarpophalangeal (MCP)joints, with subsequent development of RA orCTD. A positive rheumatoid factor had themost significant association with develop-ment of rheumatoid arthritis (no RA/CTD29% positive RF; RA/CTD 57% positive RF;P = .003).

The hazard ratio of developing 1-CA or CTDwas 2.9 in patients with positive RF com-pared with negative patients. For womenwith hand or wrist arthritis and a positive REthe hazard ratio was 8.0 compared with pa-tients with 1 fewer of these 3 features.

The survival time without development ofRA or CTD showed significant differences forthe top quartile (75% without RA or CTD) forthe clinical features of a positive RF and forinvolvement of hand joints. RF-positive pa-tients had a survival time of 32 months vs 91months for RF-negative patients. Similarly,the top quartile with involvement of theMCPs survived 35 months vs 82 monthswithout MCP arthritis.

DISCUSSION

Rheumatoid arthritis has multiple patternsof onset. This spectrum ranges between agradual onset, with small joint stiffness in-creasing over months, to an abrupt polyar-thritis with intense pain and incapacitation.

Palindromic rheumatism lies in betweenthese presentations.

Palindromic rheumatism may have featuresof many of the American Rheumatism Asso-ciation criteria (1987) for the diagnosis ofrheumatoid arthritis. This diagnosis is madeby satisfying 4 of 7 criteria, which include theclinical features of (1) polyarthritis of 3 ormore joints, (2) morning stiffness of i hour ormore, (3) symmetric arthritis, and (4) wrist,MCP, or PIP involvement. In palindromicrheumatism, these features may be presentbut only briefly, far short of the 6-week du-ration required for meeting the criteria. Theother diagnostic criteria for rheumatoid ar-thritis-(5) rheumatoid nodules, (6) a positiverheumatoid factor, and (7) radiographicchanges of periarticular joint erosion or de-calcification in the hand or wrist--need onlybe identified to meet one of the criterion.

In this study, 28% of those with palindro-mic rheumatism developed rheumatoid ar-thritis and 8% developed another connectivetissue disease. Female sex alone was not pre-dictive. Although involvement of the kneewas commonly seen, it did not discriminatethose who would evolve their palindromicrheumatism. On the other hand, 85% of thosewho developed RA or a CTD had wrist in-volvement and 71% had MCP involvement.Most predictive were the findings together offemale sex, rheumatoid factor, and wrist in-volvement.

This study also documents the time courseof palindromic rheumatism. Even in thosewith a positive rheumatoid factor and theworrisome history of episodic arthritis, itmay take years to develop rheumatoid ar-thritis.

This retrospective study is limited by thelikely referral bias inherent in universitystudies. Community patients with palindro-mic rheumatism may have less severe diseaseand be less likely to develop rheumatoid ar-thritis or another connective tissue diseasethan this study population. But as the largestcohort study of palindromic rheumatism, itidentifies risk factors for the development ofrheumatoid arthritis and other connective tis-sue disease and the course of onset.

47


LITERATURE REVIEW

Heart-Rate Recovery Immediately After Exercise as aPredictor of Mortality

Michael Moore, MD, FACP

Reference: Cole C, Blackstone E, Pashkow F, et al. Heart-rate recov-ery immediately after exercise as a predictor of mortality. N Engl JMed. 1999;341:1351-1357.

Address: Nationwide Insurance,One Nationwide Plaza, Columbus,OH 43215.

Correspondent: Michael Moore,MD, FACP, Vice President-ChiefMedical Director, Nationwide Insur-ance

Key Words: Exercise testing, heartrate recovery, mortality.



E xercise testing has long been a staple of

the requirements for many life insurersfor high-dollar life insurance policies. Therehas been considerable debate as to the use-fulness of such testing given the rather lim-ited specificity and sensitivity in those testswhich are not supplemented with either thal-lium or echocardiography. Recently therehave been several articles that have presenteddata that would seem to support the use ofthese simple, inexpensive tests as a predictorof mortality. This article is another exampleof such a study.

BACKGROUND

The expectation of exercise electrocardiog-raphy is that the heart rate will rise with in-creasing demands by increasing the elevationand speed of the treadmill. This increase isin part due to a reduction in tone from the

vagus nerve. Slowing of the heart rate follow-ing cessation of exercise is due to vagal re-activation. Poor vagal activity is known to bea risk factor for mortality, and so the cardi-ologists at the Cleveland Clinic undertook astudy to see if lack of slowing of heart ratefollowing cardiac testing could be correlatedwith increased mortality.

METHODOLOGY

A total of 2428 adults (median age 57, 63%men) without a history of heart failure, cor-onary revascularization, or pacemaker werefollowed for a period of 6 years following di-agnostic testing with SPECT exercise electro-cardiography. A failure to reduce heart rateby at least 12 beats per minute at 1 minuteinto the recovery period was considered to beabnormal.

48

MOORE--HEART-RATE RECOVERY AFTER EXERCISE

RESULTS

A total of 639 individuals met the abovedefinition of abnormal in that they did notdecrease their peak heart rate by at least 12beats per minute after 1 minute of exercisecessation.

In 6 years of the study, there were 213deaths from the 2428 total participants. Al-though only 26% (639) of the population test-ed had an abnormal result on testing, the ma-jority of the deaths (56%) occurred withinthis group. This calculates to a relative risk of4.0 for those having delayed heart rate recov-ery (confidence interval [CI] 3.0 to 5.2). Evenafter adjustments are made for age, sex, useof medications, abnormal thallium results,standard cardiac risk factors, resting heartrate, and workload achieved, the adjusted rel-ative risk factor still remained twice that ofthose who had a normal heart rate recovery(adjusted RR = 2.0; CI 1.5 to 2.7).

DISCUSSION

The lack of vagus nerve recovery followingexercise electrocardiography appears to be astrong predictor for mortality. When taken asthe only factor, failure to reduce heart rate byat least 12 beats per minute 1 minute follow-ing exercise cessation is associated with afourfold increase in risk of mortality. Evenwhen other risk factors are considered suchas the results of the SPECT exercise test, useof medicines or underlying disease, the rela-tive risk is still twice baseline.

In conclusion, lack of vagus nerve reacti-vation designated by the failure to reduce theheart rate by at least 12 beats per minute after1 minute of exercise cessation during stresselectrocardiography is an independent pre-dictor of mortality with a relative risk of 4.0and an adjusted relative risk of 2.0.

49


LITERATURE REVIEW

Glucose Intolerance and 23-Year Risk of CoronaryHeart Disease and Total Mortality

Kristi Petersen, MD

Reference: Rodrigues B, Sharp DS, Lau N, et al. Glucose intoleranceand 23-year risk of coronary heart disease and total mortality. Di-abetes Care. 1999;22:1262-1265.

Address: American United Life In-surance, One American Square, POBox 109-B C820, Indianapolis, IN46206-9101.

Correspondent: Kristi Petersen, MD,Vice President and Assistant Medi-cal Director, American United LifeInsurance.

Key words: Coronary artery heartdisease mortality, glucose intoler-ance.



I t has been well established that there is an

increased risk of total mortality and car-diovascular disease with type 2 diabetes.There is some controversy concerning the re-lationship between glucose intolerance andthese outcomes.

This study by Rodriguez et al grew out ofthe Honolulu Heart Program, which has fol-lowed 8006 men of Japanese ancestry since1965. The ages of these men ranged from 45to 68 years at study entry. Coronary heartdisease (CHD), stroke, and overall mortalitywas the study focus. The baseline examina-tion of this cohort was done between 1965and 1968 and included a medical and socio-cultural history. Habits, dietary patterns, andphysical activity were delineated. The dietaryquestionnaire looked at the extent the tradi-tional Japanese diet was followed. The phys-ical examination included body measure-

ments. Laboratory values and other screeninginformation included cholesterol, triglycer-ides, uric acid, glucose, routine urinalysis, he-matocrit, FVC, FEV1, and a resting 12-leadelectrocardiogram. A nonfasting 1-hour post-load 50-gm glucose test was used to screenthis population. It is noted that at this time,during the 1960s, these baseline laboratorystudies and this glucose challenge were con-sidered standard in epidemiologic studies. Apostload "low-normal" glucose was definedas being <150 mg/dL, "high-normal" was151-224 mg/dL, "asymptomatic high glu-cose" was considered to be >225 mg/dL, andthe "known diabetes" category consisted ofthose who reported a history of diabetes re-gardless of glucose level and were beingtreated for diabetes or who had the diagnosisof diabetes and were not being treated buthad a glucose level >225 mg/dL.

5o

PETERSEN~GLUCOSE INTOLERANCE AND MORTALITY

Age- and Risk Factor-Adjusted RR of Total Mortality, Coronary Heart Disease (CHD) incidence, and CHDmortality by Glucose Tolerance Category*

AsymptomaticVariable High Normal Hyperglycemia Known Diabetes

Total mortality

Age-adjusted 1.12 (1.02-1.23) 1.57 (1.36-1.81) 1.97 (1.70-2.30)Risk factor-adjusted~" 1.07 (0.97-1.18) 1.39 (1.20-1.61) 1.83 (1.56-2.14)

CHD incidence

Age-adjusted 1.18 (1.01-1.38) 1.68 (1.33-2.12) 2.82 (2.27-3.50)Risk factor-adjusted~ 1.08 (0.92-1.27) 1.50 (1.18-1.90) 2.26 (1.80-2.84)

CHD incidenceAge-adjusted 1.27 (0.98-1.63) 2.34 (1.70-3.24) 4.25 (3.16-5.72)Risk factor-adjusted~" 1.17 (0.91-1.50) 2.01 (1.44-2.81) 3.49 (2.56-4.75)

* Data are relative risk (95% confidence interval); low-normal group used as reference.~- Adjusted for age, pack-years of smoking, hypertension, alcohol intake, cholesterol, triglycerides, body mass index,

and Japanese diet index.

All entrants were followed through a com-prehensive hospital and death record sur-veillance system since entry into the study.Follow-up for mortality was virtually com-plete.

RESULTS

During the 23 years of follow-up, the re-suits revealed a stepwise increase in totalmortality and CHD incidence and mortalitywith worsening glucose tolerance. The asso-ciations remained significant when the riskfactors of age, smoking, alcohol intake, hy-pertension, total cholesterol, triglycerides,body mass index, and Japanese diet indexwere taken into account during the multivar-iant analysis. The study subjects that dem-onstrated low normal glucose levels wereused as reference mortality. The results areseen in the Table.

DISCUSSION

The results of this study confirm the rela-tionship between postchallenge glucose in-tolerance and coronary heart disease and to-tal mortality. The fact that this large popu-lation-based study did not use what we nowconsider the "gold standard" oral glucose tol-

erance test--ie, a fasting 2-hour glucose mea-surement after a 75-gm glucose load--is a po-tential limitation. It is possible that a strongerassociation between glucose tolerance, CHD,and total mortality would be observed if ourcurrent screening methods had been used.The screening technique also may have intro-duced enough variation to account for thefailure to show an association between highnormal glucose levels, CHD, and mortality,after the adjustment for risk factors was done.

In the insurance industry, we cannot alwaysbe assured that the client will be fasting whenthe blood is drawn for the required laboratoryexamination. If I may draw on clinical practiceexperience, few patients count coffee, softdrinks, or even toast or a bagel as breaking afast. I would maintain that the screening tech-nique used in this study is equivalent to ourapplicant population when they have a para-medical exam for insurance purposes. A 50-gm glucose load in a nonfasting study entrantis nearly the same as a nonfasting applicantwho drinks I soft drink prior to a blood drawfor an insurance laboratory. This study hasmore relevance to the insurance industry thaninitially might be thought: the glucose level ispertinent to risk assessment no matter whatour clients consider to be fasting.

51


LITERATURE REVIEW

Cardiorespiratory Fitness and Mortality in Men

John Kirkpatrick, MA, MD

Reference: Wei M, Kampert J, Barlow C, et al. Relationship betweenlow cardiorespiratory fitness and mortality in normal-weight, over-weight, and obese men. JAMA. 1999;282:1547-1553.

Address: Aid Association for Lu-therans, 4321 N Ballard Road, Ap-pleton, WI 54919-0001.

Correspondence: John E. Kirkpa-trick, MD, 2nd Vice President andAssociate Medical Director.

Key Words: Cardiorespiratory fit-ness, obesity, mortality.



T he prevalence of obesity is increasing inthe United States. This substantial in-

crease had lead some to consider obesity asa modem epidemic. The correlation betweenobesity and mortality is certainly not a newone. This study attempts to address low car-diorespiratory fitness as an independent vari-able for cardiovascular disease deaths and all-cause mortality.

The data from this study are based on theAerobics Center Longitudinal Study, a studyassociated with Kenneth Cooper and the Coo-per Institute. They collected 25,714 patientsover the period 1970-1993. The populationwas all male; 95% were white, and 80% werecollege graduates. Most were executives orprofessionals and considered to be in themid- to upper socioeconomic strata.

The follow-up was "approximately 10years," although a minimum period of I yearwas required. The population was catego-rized by body mass index (BMI). Normalweight was considered to be a BMI of 18.5 to24.9. Overweight was defined as a BMI of 25

to 29.9, and obesity was considered to be aBMI of >30.

The authors included 6 "mortality predic-tors" as study variables. Two of the mortalitypredictors were disease conditions; the pres-ence of cardiovascular disease (CVD) and di-abetes mellitus. The other 4 were increasedserum cholesterol, hypertension, smoking,and low cardiovascular fitness. Cardiovascu-lar fitness was determined by performance ona maximal exercise test on a treadmill. Sub-sets were defined by a MET cutoff point forlow fitness: ages 20-39, 10.5 METS; ages 40-49, 9.9 METS; ages 50-59, 8.8 METS; and age>60, 7.5 METS.

There were 1025 deaths during the 258,781man-years of follow-up. There were 439deaths due to CVD, 43% of total deaths ex-perienced. The baseline characteristics of theobese subset were that they had higher cho-lesterol lower exercise tolerance, higher bloodpressure, higher rate of physical inactivity, in-creased diabetes mellitus, and increased rateof CVD. The study calculated the relative risk

52

KIRKPATRICK--CARDIORESPIRATORY FITNESS AND MORTALITY

(RR) of CVD deaths and all-cause mortalityas compared to the normal weight group. Ascompared with the normal weight groupwith no CVD, obese patients with a historyof CVD have a RR of 14.0 for CVD death. Thepresence of any of the individual mortalitypredictors studied increased the age adjustedRR for CVD deaths by 4.4 to 5.0 (as comparedwith the normal weight group without thatparticular variable). There was a very strongtrend of increased mortality as the BMI in-creased. All-cause mortality showed a similartrend. The presence of CVD was the strongestsingle variable in increasing the RR of all-cause mortality. The other 5 predictorsshowed an increase in RR from 2.7 to 3.1 inall-cause mortality (as compared with thenormal-weight subset without that particularvariable). In multivariate analysis, baselineCVD remained the most significant variable,as expected. The other 5 were similar in their

influence on CVD death and all-cause mor-tality.

There are weaknesses to this study. Thenumber of patients accumulated is impres-sive; however, the population was quite ho-mogenous. Entrants were well-educated,white men in a high socioeconomic strata.The referral center is a unique facility wellknown for its emphasis on fitness. Whetheror not these results can be reproduced in amore normal clinical setting should be pur-sued.

The conclusions of the study, given theselimitations, are worthy of a trend impression.It is clear that as as patients progress in BMIfrom normal to obese, there is a significantincrease in both CVD deaths and all-causemortality. The presence of CVD remains themost significant factor. Low cardiovascularfitness was as significant a factor as diabetesmellitus, increased cholesterol, hypertensionand smoking.

53

effect of cigar smoking on the risk of cardiovascular...

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