Pierre Biron

Familial resemblance of body weight and weight/height in 374 homes with adopted children.

Body weight and weight/height were measured in 535 children adopted at the median age of 3 months, and in 250 natural children in French-Canadian origin living in 374 Montreal homes, to determine whether the shared environment contributed to the familial resemblance of weight in children aged one to 21. The mid-parent vs natural childrens correlation ( r2 X 100) was 9.55% for body weight and 6.60% for W/H (p less than 0.01), whereas the mid-parent vs adopted childrens correlation was 0.00% for both characteristics. The sib-sib correlation in 80 homes with greater than 1 natural child was 15.2% for weight and 13.48% for W/H (p less than 0.001), whereas in 138 homes with greater than 1 adopted child, the adoptee-adoptee correlations were, respectively, 0.00% and 0.07%. It is concluded that heredity explains most of the familial aggregation of patterns of weight and weight/height in children. This conclusion does not necessarily apply to obesity, since weight indices in children do not accurately reflect excess fat tissue, and half of the adoptees were adopted after the age of three months.

Captopril in infants for congestive heart failure secondary to a large ventricular left-to-right shunt

Abstract Vasodilators have been used for many years in the treatment of cardiac failure of adult patients with cardiomyopathy, mitral regurgitation or coronary artery disease. More recently, they have been used in children with similar problems.1,2 Their use in infants with ventricular left-to-right shunts was suggested a few years ago3 but did not gain wide acceptance. One of the reasons could be the difficulty of finding a safe and reliable systemic vasodilator that could be administered orally in infants. This study investigates the ability of captopril, a selective systemic vasodilator, to reduce ventricular leftto-right shunting and assesses the global hemodynamic status of infants receiving the drug.

THE INFLUENCE OF GENETICS AND HOUSEHOLD ENVIRONMENT UPON THE VARIABILITY OF NORMAL BLOOD PRESSURE: THE MONTREAL ADOPTION SURVEY

The Montreal Adoption Survey was conducted as a cross-sectional epidemiologic study of cardiovascular risk factors in French Canadian families. Analysis included blood pressure readings of 756 adopted and 445 natural children as well as 1176 parents. A genetic model was applied to the analysis of our data. Interindividual variability of blood pressure was studied and observed correlatives of systolic and diastolic pressure of parental and non parental subjects were calculated. Based on the maximum likelihood estimates presented in the models the explanation of the parent offspring and the between sibs expected population correlatives for systolic blood pressure was the following: 61% was due to shared genes and 39% to environment shared by both parents and children. For diastolic blood pressure the explanation between parents and offspring was the following: 58% was due to shared genes and 42% due to shared environment across generation. The explanation between sibs was estimated to be the following: 33% due to generation, 24% to shared environment across generation and 43% to shared environment within generation.

Familial aggregation of blood pressure and its components.

The well known existence of familial clustering of blood pressure among adults raises two important questions: At what age does this aggregation become significant? Are either shared environment or heredity or both the responsible components?

Fate of angiotensin I and II in the human pulmonary circulation

Abstract The systemic pressure response technic was applied in 4 patients undergoing diagnostic catheterization. Injections were made alternately into the pulmonary artery and the ascending aorta and the systemic arterial pressor responses to each of these two routes of administration were compared. In 2 subjects, the pressor potency of angiotensin II given by way of the pulmonary artery was identical to that resulting from aortic injections, thus indicating the absence of pulmonary extraction of the octapeptide. In 2 other patients, angiotensin I was twice as potent by the pulmonary than by the aortic route; this could have resulted only from the marked conversion of the inactive decapeptide under the influence of pulmonary converting-enzyme activity. These data provide the clinical confirmation of previous animal observations pointing to the important role played by the lungs in the renin-angiotensin system. Application of the systemic pressure response technic has proved to be easy and safe during cardiac catheterization in man, and it can now be used to study the fate of vasoactive drugs or hormones in the pulmonary circulation.

Point: Why statins have failed to reduce mortality in just about anybody

This discussion was sparked by an editorial critique by Sniderman et al regarding the 2010 Cholesterol Treatment Trialists’ (CTT) meta-analysis that suggested a statin ‘‘event’’ benefit from maximal lowering of low-density lipoprotein cholesterol levels. There are two issues that deserve further attention: the components of the CTT study end points and, most importantly, the issue of reduction in all-cause mortality.

Acebutolol: Basis for the prediction of effect on exercise tolerance

Twelve unselected males suffering from documented coronary insufficiency and moderately severe angina were submitted to graded multistage treadmill exercise testing on 3 separate days, 3.5 hr after a single dose of 0, 200, or 400 mg of acebutolol, a cardioselective beta blocker. Control measures included random allocation of 2 patients to each of 6 balanced sequences of administration, standardized double‐blind conditions, and variance analysis for Latin‐square design with repeated measures on each subject. Performance was evaluated by measuring time elapsed until anginal pain, peak heart rate, peak product of heart rate and blood pressure, and peak oxygen consumption. Mean values for all criteria were significantly altered by 400 mg of acebutolol. Seven out of twelve patients were classified as responders (i.e., exercise duration increased 100% or more). The response after acebutolol was correlated with the performance on placebo in the case of exercise duration, peak heart rate, and peak product of heart rate and blood pressure. It is concluded that: (1) performance criteria are useful predictors of response to beta blockade and (2) acebutolol is a potent antianginal agent when judged by an objective treadmill exercise test.

Letter by Vos et al Regarding Article, “Primary Prevention With Statin Therapy in the Elderly: New Meta-Analyses From the Contemporary JUPITER and HOPE-3 Randomized Trials”

We read with interest the article by Ridker et al1 that proposes, based on 2 rosuvastatin trials, JUPITER (Justification for Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin) and HOPE-3 (Heart Outcomes Prevention Evaluation), that there would be a probable statin mortality benefit in primary prevention in the elderly.2,3 The article relies on the combined end point of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death, but without separating these …

Blood pressure drugs have no mortality benefit in diabetic patients

To the Editor: We question the following statement in the article by Campbell et al (1): “Treatment of high blood pressure in people with diabetes results in large reductions in death...within a short period of time...” This statement was based on references 2 to 10. However, the first two references (2,3) found no mortality benefit from these angiotensin receptor blockers. The next reference (4) reported a nonsignificant mortality difference after nine years from “tight blood pressure control”. Reference 5 is a subgroup of the Appropriate Blood Pressure Control in Diabetes (ABCD) trial. This trial showed no mortality benefit (P=0.8) from aggressive blood pressure control after 5.3 years, while reference 6 represented the balance of ABCD participants – those with higher baseline blood pressure – and demonstrated borderline significant mortality benefit (the given P=0.037 was erroneous). The Action in Diabetes and Vascular Disease: Preterax and Diamicron MR Controlled Evaluation (ADVANCE) trial (7) reported P=0.03 for mortality, but 79 diabetic patients would have to take perindopril plus indapamide for five years to postpone the death of one patient (78 representing the number needlessly treated). The Micro Heart Outcomes Prevention Evaluation (MICRO-HOPE) substudy (8) found a nonsignificant mortality difference emerging after two years on ramipril, and 31 diabetic patients would have to take this drug for 4.5 years to postpone one death. Interestingly, the authors propose that much of the action of this angiotensin-converting enzyme inhibitor may be from mechanisms other than those that lower blood pressure (11). The Systolic Hypertension in Europe (Syst-Eur) trial (9) reported no significant mortality benefit (P=0.09) from calcium channel blockade after two years. Ominously, the study mentioned potential harm from calcium channel blockers in diabetic patients. Reference 10 was a meta-analysis of diabetic and nondiabetic patients suffering a total of 17,000 major cardiovascular events. In the diabetic patients, the above angiotensin receptor blocker and angiotensin-converting enzyme inhibitor effects were reflected, but because treatment durations were not given, numbers needed or needlessly treated cannot be calculated. The authors, therefore, are not supported by evidence when suggesting short-term “major reductions in death”, and diabetic patients must be told. What is urgently needed are numbers needed or needlessly treated for individual end points – ie, death, ischemic (nontransient ischemic attack) and hemorrhagic stroke, myocardial infarction, heart and kidney failure and microangiopathies – for each of the available blood pressure drugs, for one to five years of treatment, rather than ‘relative combined end point risk reductions’ without defined treatment periods. With such numbers needed or needlessly treated (and it is likely that none of them are less than 100 patient treatment-years per end point, which in itself, would make clinical relevance doubtful), we can clearly inform patients and consider other avenues to tackle diabetes, which, after all, is mostly a preventable metabolic disease (insulin resistance secondary to excess visceral fat due to junk food addiction) and of which blood pressure can be a symptom but not the cause.