Light cigarette smoking and Cardiovascular diseases

Light cigarette smoking impairs coronary microvascular functions as severely as smoking regular cigarettes

Hakan Gullu, Mustafa Caliskan, Ozgur Ciftci, Dogan Erdogan, Semra Topcu, Erkan Yildirim, Aylin Yildirir, Haldun Muderrisoglu
1 ) Baskent University, Faculty of Medicine, Cardiology Department, Ankara, Turkey; 
2) Baskent University, Faculty of Medicine, Radiology Department, Ankara, Turkey

Background: Smoking is the most prevalent and most preventable risk factor for cardiovascular diseases. Smoking low-tar, low-nicotine cigarettes (light cigarettes) would be expected to be less hazardous than smoking regular cigarettes owing to the lower nicotine and tar yield.

Objective: To compare the chronic and acute effects of light cigarette and regular cigarette smoking on coronary flow velocity reserve (CFVR).

Methods: 20 regular cigarette smokers (mean (SD) age 24.8 (5.0)), 20 light cigarette smokers (mean age 25.6 (6.4)), and 22 non-smoker healthy volunteers (mean age 25.1 (4.2)) were included. First, each subject underwent echocardiographic examination, including CFVR measurement, after a 12 hour fasting and smokeless period. Two days later, each subject smoked two of their normal cigarettes in a closed room within 15 minutes. Finally, within 20–30 minutes, each subject underwent an echocardiographic examination, including CFVR measurement.

Results: Mean (SD) CFVR values were similar in light cigarette and regular cigarette smokers and significantly lower than in the controls (2.68 (0.50), 2.65 (0.61), 3.11 (0.53), p = 0.013). Before and after smoking a paired t test showed that smoking two light cigarettes acutely decreased the CFVR from 2.68 (0.50) to 2.05 (0.43) (p = 0.001), and smoking of two regular cigarettes acutely decreased CFVR from 2.65 (0.61) to 2.18 (0.48) (p = 0.001).

Conclusion: Our study suggest that reducing the nicotine and tar yield is not sufficient for a cigarette to be called less hazardous, and other noxious compounds in cigarettes continue to compromise human health. Smoking low-tar, low-nicotine cigarettes seems to have the same unfavourable effect on the coronary microvascular functions as smoking regular cigarettes. Action should be taken to prohibit misleading terminology such as "light".

Heart 2007;93:1274-1277
http://heart.bmj.com/cgi/content/abstract/93/10/1274
© 2007 BMJ Publishing Group Ltd & British Cardiovascular Society

Septic myocardial dysfunction

Sepsis and the Heart

M.W. Merx, MD; C. Weber, MD
From the Department of Medicine (M.W.M.), Division of Cardiology, Pulmonary Diseases and Vascular Medicine and the Institute of Molecular Cardiovascular Research (IMCAR) at the University Hospital (C.W.), RWTH Aachen University, Aachen, Germany.

Sepsis is generally viewed as a disease aggravated by an inappropriate immune response encountered in the afflicted individual.
As an important organ system frequently compromised by sepsis and always affected by septic shock, the cardiovascular system and its dysfunction during sepsis have been studied in clinical and basic research for more than 5 decades.
Although a number of mediators and pathways have been shown to be associated with myocardial depression in sepsis, the precise cause remains unclear to date.
There is currently no evidence supporting global ischemia as an underlying cause of myocardial dysfunction in sepsis; however, in septic patients with coexistent and possibly undiagnosed coronary artery disease, regional myocardial ischemia or infarction secondary to coronary artery disease may certainly occur.
A circulating myocardial depressant factor in septic shock has long been proposed, and potential candidates for a myocardial depressant factor include cytokines, prostanoids, and nitric oxide, among others.
Endothelial activation and induction of the coagulatory system also contribute to the pathophysiology in sepsis. Prompt and adequate antibiotic therapy accompanied by surgical removal of the infectious focus, if indicated and feasible, is the mainstay and also the only strictly causal line of therapy. In the presence of severe sepsis and septic shock, supportive treatment in addition to causal therapy is mandatory.
The purpose of this review is to delineate some characteristics of septic myocardial dysfunction, to assess the most commonly cited and reported underlying mechanisms of cardiac dysfunction in sepsis, and to briefly outline current therapeutic strategies and possible future approaches.

Key Words: immune system • infection • inflammation • shock • sepsis

Circulation. 2007;116:793-802.
© 2007 American Heart Association, Inc.

Body Mass Index in Patients with Chronic Heart Failure

Body Mass Index and Prognosis in Patients With Chronic Heart Failure: Insights From the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) Program

Satish Kenchaiah, MD, MPH; Stuart J. Pocock, PhD; Duolao Wang, PhD at al.

Background. In individuals without known cardiovascular disease, elevated body mass index (BMI) (weight/height2) is associated with an increased risk of death. However, in patients with certain specific chronic diseases, including heart failure, low BMI has been associated with increased mortality.

Methods and Results. We examined the influence of BMI on prognosis using Cox proportional hazards models in 7599 patients (mean age, 65 years; 35% women) with symptomatic heart failure (New York Heart Association class II to IV) and a broad spectrum of left ventricular ejection fractions (mean, 39%) in the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) program. During a median follow-up of 37.7 months, 1831 patients died. After adjustment for potential confounders, compared with patients with BMI between 30 and 34.9, patients in lower BMI categories had a graded increase in the risk of death. The hazard ratios (95% confidence intervals) were 1.22 (1.06 to 1.41), 1.46 (1.24 to 1.71), and 1.69 (1.43 to 2.01) among those with BMI of 25 to 29.9, 22.5 to 24.9, and <22.5,>0.20). However, lower BMI was associated with a greater risk of all-cause death in patients without edema but not in patients with edema (P for interaction <0.0001). Lower BMI was associated with a greater risk of cardiovascular death and noncardiovascular death. Baseline BMI did not influence the risk of hospitalization for worsening heart failure or due to all causes.

Conclusions. In patients with symptomatic heart failure and either reduced or preserved left ventricular systolic function, underweight or low BMI was associated with increased mortality, primarily in patients without evidence of fluid overload (edema).

Circulation. 2007;116:627-636.
© 2007 American Heart Association, Inc.

HRQL in cardiac patients

Poor Health-Related Quality of Life Is a Predictor of Early, But Not Late, Cardiac Events After Percutaneous Coronary Intervention

Susanne S. Pedersen, Ph.D., Elisabeth J. Martens, Ph.D., Johan Denollet, Ph.D., and Ad Appels, Ph.D.
From CoRPS–Center of Research on Psychology in Somatic diseases, Tilburg Univ., The Netherlands; Dept. of Medical Psychology, Maastricht Univ., The Netherlands. Send correspondence and reprint requests to Susanne S. Pedersen, Ph.D., CoRPS, Dept. of Medical Psychology, Room P503a, Tilburg Univ., Warandelaan 2, PO Box 90153, 5000 LE Tilburg, The Netherlands.

Poor health-related quality of life (HRQL) is associated with mortality in cardiac patients.

Patients (N=667) with poor HRQL after percutaneous coronary intervention had a higher incidence of early ( 6 months) major adverse cardiac events (MACE) than did patients with good HRQL, whereas there was no difference for late (>6 months) MACE over a 2-year follow-up period.

Poor HRQL remained an independent predictor of early, but not late MACE, adjusting for other risk factors. The same pattern was found for early and late death/non-fatal myocardial infarction.

However, further research is warranted before recommending the use of HRQL measures as screening tools in clinical practice. Full Text

Psychosomatics 48:331-337, August 2007

© 2007 Academy of Psychosomatic Medicine

Circadian rhythm and Coronary death

When Throughout the Year Is Coronary Death Most Likely to Occur?
A 12-Year Population-Based Analysis of More Than 220 000 Cases

Robert A. Kloner, MD, PhD; W. Kenneth Poole, PhD; Rebecca L. Perritt, MS
From the Heart Institute Research Laboratory, Good Samaritan Hospital and Section of Cardiology, University of Southern California (R.A.K.), Los Angeles, Calif, and Research Triangle Institute, Research Triangle, NC (W.K.P., R.L.P.).

Background. Previous studies have suggested that there is an increase in cardiac events in the morning. Fewer data relate cardiac events to months of the year and season.

Methods and Results. We analyzed all monthly death certificate data from Los Angeles County, California, for death caused by coronary artery disease from 1985 through 1996 (n=222 265). The mean number of deaths was highest in December at 1808 and January at 1925; the lowest rates were in June, July, August, and September at 1402, 1424, 1418, and 1371, respectively. December and January had significantly higher rates than would be expected from a uniform distribution of monthly deaths (P=0.00001). The percent of yearly coronary deaths was defined by the quadratic U-shaped equation [percent=13.1198-1.5238(month)+0.0952(month2), where January=1, February=2, etc]. When monthly deaths were plotted by year, there was a decrease from 1985 through 1996. Monthly mortality correlated inversely with temperature. During the months with the highest frequency of death (December, January), however, there was an increase in deaths that peaked around the holiday season and then fell, which could not be explained solely on the basis of the daily temperature change.

Conclusions. Even in the mild climate of Los Angeles County, there are seasonal variations in the development of coronary artery death, with 33% more deaths occurring in December and January than in June through September. Although cooler temperatures may play a role, other factors such as overindulgence or the stress of the holidays might also contribute to excess deaths during these peak times.

Key Words: cardiovascular diseases • circadian rhythm • coronary disease • death, sudden • heart diseases

Circulation. 1999;100:1630-1634.
© 1999 American Heart Association, Inc.

Cocoa may lower blood pressure

Cocoa, but not tea, may lower blood pressure

Current guidelines advise individuals with hypertension (high blood pressure) to eat more fruits and vegetables, according to background information in the article. Compounds known as polyphenols or flavonoids in fruits and vegetables are thought to contribute to their beneficial effects on blood pressure and cardiovascular risk. "Tea and cocoa products account for the major proportion of total polyphenol intake in Western countries," the authors write. "However, cocoa and tea are currently not implemented in cardioprotective or anti-hypertensive dietary advice, although both have been associated with lower incidences of cardiovascular events."

Dirk Taubert, M.D., Ph.D., and colleagues at the University Hospital of Cologne, Germany, conducted a meta-analysis of 10 previously published trials, five of cocoa's effects on blood pressure and five involving tea. All results were published between 1966 and 2006, involved at least 10 adults and lasted a minimum of seven days. The studies were either randomized trials, in which some participants were randomly assigned to cocoa or tea groups and some to control groups, or used a crossover design, in which participants' blood pressure was assessed before and after consuming cocoa products or tea.

The five cocoa studies involved 173 participants, including 87 assigned to consume cocoa and 86 controls, 34 percent of whom had hypertension (high blood pressure). They were followed for a median (middle) duration of two weeks. Four of the five trials reported a reduction in both systolic (the top number, when the heart contracts) and diastolic (the bottom number, when the heart relaxes) blood pressure. Compared with those who were not consuming cocoa, systolic blood pressure was an average of 4.7 millimeters of mercury lower and diastolic blood pressure was an average of 2.8 millimeters of mercury lower.

The effects are comparable to those achieved with blood pressure-lowering medications, the authors note. "At the population level, a reduction of 4 to 5 millimeters of mercury in systolic blood pressure and 2 to 3 millimeters of mercury in diastolic blood pressure would be expected to substantially reduce the risk of stroke (by about 20 percent), coronary heart disease (by 10 percent) and all-cause mortality (by 8 percent)," they write.

Of the 343 individuals in the five tea studies, 171 drank tea and 172 served as controls, for a median duration of four weeks. Drinking tea was not associated with a reduction in blood pressure in any of the trials.

Tea and cocoa are both rich in polyphenols, but while black and green tea contain more compounds known as flavan-3-ols, cocoa contains more of another type of polyphenol, procyanids. "This suggests that the different plant phenols must be differentiated with respect to their blood pressure-lowering potential and thus cardiovascular disease prevention, supposing that the tea phenols are less active than cocoa phenols," the authors write.

The findings do not indicate a widespread recommendation for higher cocoa intake to decrease blood pressure, but it appears reasonable to substitute phenol-rich cocoa products such as dark chocolate for other high-calorie or high-fat desserts or dairy products, they continue. "We believe that any dietary advice must account for the high sugar, fat and calorie intake with most cocoa products," the authors conclude. "Rationally applied, cocoa products might be considered part of dietary approaches to lower hypertension risk."

JAMA and Archives Journals, April 10, 2007
http://www.brightsurf.com/news/

Genetic determinants of hemodynamic and chronotropic responses

Heritability, Linkage, and Genetic Associations of Exercise Treadmill Test Responses

Erik Ingelsson, MD, PhD; Martin G. Larson, ScD; Ramachandran S. Vasan, MD*; Christopher J. O’Donnell, MD, MPH; Xiaoyan Yin, MS; Joel N. Hirschhorn, MD, PhD; Christopher Newton-Cheh, MD, MPH; Jared A. Drake, BA; Stacey L. Musone, BA; Nancy L. Heard-Costa, PhD; Emelia J. Benjamin, MD, ScM; Daniel Levy, MD; Larry D. Atwood, PhD; Thomas J. Wang, MD; Sekar Kathiresan, MD

Background. The blood pressure (BP) and heart rate responses to exercise treadmill testing predict incidence of cardiovascular disease, but the genetic determinants of hemodynamic and chronotropic responses to exercise are largely unknown.

Methods and Results. We assessed systolic BP, diastolic BP, and heart rate during the second stage of the Bruce protocol and at the third minute of recovery in 2982 Framingham Offspring participants (mean age 43 years; 53% women). With use of residuals from multivariable models adjusted for clinical correlates of exercise treadmill testing responses, we estimated the heritability (variance-components methods), genetic linkage (multipoint quantitative trait analyses), and association with 235 single-nucleotide polymorphisms in 14 candidate genes selected a priori from neurohormonal pathways for their potential role in exercise treadmill testing responses. Heritability estimates for heart rate during exercise and during recovery were 0.32 and 0.34, respectively. Heritability estimates for BP variables during exercise were 0.25 and 0.26 (systolic and diastolic BP) and during recovery, 0.16 and 0.13 (systolic and diastolic BP), respectively. Suggestive linkage was found for systolic BP during recovery from exercise (locus 1q43–44, log-of-the-odds score 2.59) and diastolic BP during recovery from exercise (locus 4p15.3, log-of-the-odds score 2.37). Among 235 single-nucleotide polymorphisms tested for association with exercise treadmill testing responses, the minimum nominal probability value was 0.003, which was nonsignificant after adjustment for multiple testing.

Conclusions. Hemodynamic and chronotropic responses to exercise are heritable and demonstrate suggestive linkage to select loci. Genetic mapping with newer approaches such as genome-wide association may yield novel insights into the physiological responses to exercise.

Circulation. 2007;115:2917-2924.
© 2007 American Heart Association, Inc.
http://circ.ahajournals.org/cgi/content/abstract/115/23/2917