World No Tobacco Day

World No Tobacco Day is observed around the world every year on May 31. The member states of the World Health Organization created World No Tobacco Day in 1987. It draws global attention to the tobacco epidemic and to the preventable death and disease it causes. It aims to reduce the 3.5 million yearly deaths from tobacco related health problems.

History

• In 1987, the World Health Assembly passed Resolution WHA40.38, calling for April 7, 1988 to be "a world no-smoking day."
• In 1988, Resolution WHA42.10 was passed, calling for the celebration of World No Tobacco Day, every year on 31 May.

The health effects of tobacco smoking refer to direct tobacco smoking as well as the inhalation of environmental or secondhand tobacco smoke. The WHO in the 2002 World Health Report estimates that in developed countries, 26% of male deaths and 9% of female deaths can be attributed to smoking. Similarly, the United States'

Centers for Disease Control and Prevention describes tobacco use as "the single most important preventable risk to human health in developed countries and an important cause of premature death worldwide".

Primary risks

The main health risks in tobacco pertain to diseases of the cardiovascular system, in particular smoking being a major risk factor for amyocardial infarction (heart attack), diseases of the respiratory tract such as Chronic Obstructive Pulmonary Disease (COPD) and emphysema, and cancer, particularly lung cancer and cancers of the larynx and mouth. Prior to World War I, lung cancer was considered to be a rare disease, which most physicians would never see during their career. With the postwar rise in popularity of cigarette smoking came a virtual epidemic of lung cancer.

Incidence of impotence is approximately 85 percent higher in male smokers compared to non-smokers, and it is a key cause of erectile dysfunction (ED). Smoking causes impotence because it promotes arterial narrowing. Tobacco related illnesses kill 440,000 USA citizens per year, about 1,205 per day, making it the leading cause of preventable death in the U.S. A person's increased risk of contracting disease is directly proportional to the length of time that a person continues to smoke as well as the amount smoked. However, if someone stops smoking, then these chances gradually decrease as the damage to their body is repaired.

Diseases linked to smoking tobacco cigarettes include:

• Most forms of cancer, particularly lung cancer, cancer of the kidney, cancer of the larynx and head and neck, bladder, esophagus, pancreas, and stomach. There is some evidence suggesting an increased risk of myeloid leukemia, squamous cell sinonasal cancer, liver cancer, cervical cancer, colorectal cancer after an extended latency, childhood cancers and cancers of the gall bladder, adrenal gland and small intestine.
• Cardiovascular diseases
• Stroke
• Respiratory ailments such as the common cold and bronchitis
• Peripheral vascular diseases
• Birth defect of pregnant smokers' offspring
• Buerger's disease (thromboangiitis obliterans)
• Impotence
• Chronic obstructive pulmonary disease, emphysema and chronic bronchitis in particular
• More likely to develop cataracts that may cause blindness
• Reduced memory and cognitive abilities in adolescent smokers (Biol Psychiatry. 2005 Jan 1;57(1):56-66)

Ambulatory Arterial Stiffness Index

Ambulatory Arterial Stiffness Index Is Not a Specific Marker of Reduced Arterial Compliance

Giuseppe Schillaci; Gianfranco Parati; Matteo Pirro; Giacomo Pucci; Massimo R. Mannarino; Laura Sperandini; Elmo Mannarino
From the Unit of Internal Medicine (G.S., M.P., G.Pucci, M.R.M., L.S., E.M.), Angiology and Arteriosclerosis, University of Perugia, Perugia, Italy; the Department of Clinical Medicine and Prevention (G.Parati), University of Milano-Bicocca, Milan, Italy; and the Department of Cardiology (G.Parati), San Luca Hospital, IRCCS, Istituto Auxologico Italiano, Milan, Italy

Ambulatory arterial stiffness index (AASI), a measure based on the relative behavior of 24-hour systolic and diastolic blood pressure (BP), has been suggested as a marker of arterial stiffness and a predictor of cardiovascular mortality.

However, a narrow range of diastolic BP values over the 24 hours tends to flatten the regression slope and to artificially increase AASI. We explored the possible influence of different ranges of 24-hour diastolic BP fluctuations, such as those related to nocturnal BP fall, on AASI, and on its relationship with target organ damage. In 515 untreated hypertensive patients, AASI was directly related to age (r=0.30) and 24-hour systolic BP (r=0.20), whereas it was inversely related with nocturnal systolic and diastolic BP reduction (r=–0.28 and –0.46, respectively; all P<0.001). r="0.17;" r="0.28;">

Our conclusions are as follows: (1) AASI is strongly dependent on the degree of nocturnal BP fall in hypertensive patients; (2) there is no significant relation between AASI and left ventricular mass after proper adjustment for confounders; and (3) the relation between AASI and a widely accepted measure of aortic stiffness, such as pulse wave velocity, is weak and importantly affected by other factors.

Key Words: ambulatory blood pressure monitoring • arteries • blood pressure • arterial stiffness • left ventricular hypertrophy

Hypertension. 2007;49:986.

© 2007 American Heart Association, Inc.

Hypertension - Smoking: Impact and Cessation

Impact of Smoking and Smoking Cessation on Arterial Stiffness and Aortic Wave Reflection in Hypertension

Noor A. Jatoi; Paula Jerrard-Dunne; John Feely; Azra Mahmud
From the Department of Pharmacology and Therapeutics, Trinity College Dublin, Trinity Centre, St James’s Hospital, Dublin, Ireland.

Cigarette smoking is an important modifiable cardiovascular risk factor and pathophysiological mechanisms may include a stiff vascular tree. Although smokers have stiffer arteries, whether smoking cessation is associated with reduced arterial stiffness is not known.
We compared never-treated patients with essential hypertension (n=554) aged 18 to 80 years (56% females) classified as current smokers (n=150), ex-smokers (n=136), and nonsmokers (n=268). Ex-smokers were categorized into <1>1 and <10>10 years of smoking cessation.
Measurements included aortic stiffness, assessed as pulse wave velocity (Complior), wave reflection (augmentation index [AIx]), and transit time (TR) (Sphygmocor).
Current and ex-smokers had significantly higher pulse wave velocity and AIx compared with nonsmokers (pulse wave velocity for current smokers: 10.7±0.2; ex-smokers: 10.6±0.2; nonsmokers: 9.9±0.1 m/s; P<0.001; AIx for current smokers: 31±1; ex-smokers: 30±1; nonsmokers: 27±0.8%; P<0.05), whereas TR was lower in current and ex-smokers compared with nonsmokers (TR for current smokers: 131±1.0; ex-smokers: 135±1; nonsmokers: 137±0.8 m/s; P<0.0001).
There was a significant linear relationship between smoking status and pulse wave velocity (P<0.001), AIx (P<0.001), and TR (P<0.001), even after adjusting for age, sex, mean arterial pressure, heart rate, and body mass index.
In ex-smokers, duration of smoking cessation had a significant linear relationship with improvement in pulse wave velocity (P<0.001), AIx (P<0.001), and TR (P<0.001), with arterial stiffness parameters returning to nonsignificant levels after a decade of smoking cessation.

Key Words: smoking • arterial stiffness • pulse wave velocity • augmentation index • hypertension • smoking cessation

Hypertension. 2007;49:981.
© 2007 American Heart Association, Inc
http://hyper.ahajournals.org/cgi/content/abstract/49/5/981

Hypertension: Gene Pathways to New Therapies

Molecular Genetics of Experimental Hypertension and the Metabolic Syndrome
From Gene Pathways to New Therapies

Michal Pravenec; Theodore W. Kurtz
From the Institute of Physiology and Center for Applied Genomics (M.P.), Czech Academy of Sciences, Prague, Czech Republic; and the Department of Laboratory Medicine (T.W.K.), University of California San Francisco

Genetic studies of human and experimental hypertension provide a means to identify key pathways that predispose individuals to increased blood pressure and associated risk factors for cardiovascular and metabolic diseases.

The pathways so identified can then serve as targets for therapeutic intervention. This article discusses genetic studies in animal models of hypertension in which specific genes have been identified that regulate blood pressure and biochemical features of the metabolic syndrome.

Consistent with studies in humans with monogenic disorders of blood pressure regulation, studies in rat models have demonstrated that naturally occurring genetic variation in pathways regulating sodium chloride transport can contribute to inherited variation in blood pressure.

Such studies have also indicated that naturally occurring variation in genes, such as Cd36, that regulate fatty acid metabolism and ectopic accumulation of fat and fat metabolites can influence both biochemical and hemodynamic features of the metabolic syndrome and mediate the antidiabetic effects of drugs that activate the peroxisome proliferator-activated receptor . Angiotensin II receptor blockers with the ability to selectively modulate activity of peroxisome proliferator-activated receptor and expression of genes in these fat metabolism pathways may represent useful prototypes for a new class of transcription modulating drugs aimed at treating patients with hypertension and the metabolic syndrome.

Key Words: genetics • rats • inbred SHR • metabolic syndrome X • hypertension • angiotensin II type 1 receptor blockers • peroxisome proliferator-activated receptors

Hypertension. 2007;49:941.

© 2007 American Heart Association, Inc

Fontan Conversion - Effective Alternative

Fontan Conversion Still An Effective Alternative

Fontan conversion accompanied by arrhythmia surgery and pacemaker implantation remains a safe and effective alternative to cardiac transplantation for patients with failing Fontan circulation, Dr. Constantine Mavroudis reported at the annual meeting of the Society of Thoracic Surgeons.
During the past several years patients with failing Fontans have been presenting at an older age, with more complex lesions and more-difficult-to-manage atrial arrhythmias as the increasing popularity of transcatheter ablation procedures has delayed surgical referral.
Yet results remain excellent due to evolution in surgical techniques and advances in pacemaker therapy, said Dr. Mavroudis, the Willis J. Potts Professor of Surgery at Northwestern University and surgeon-in-chief at Children's Memorial Hospital, Chicago.
His retrospective study examined 111 consecutive patients who underwent atriopulmonary to total cavopulmonary artery extracardiac Fontan conversion at the hospital since late 1994.
The patients' mean age was 23 years, with a mean 14-year interval between Fontan and Fontan conversion. Fourteen patients had undergone prior Fontan revisions.
Dr. Mavroudis divided the experience into three periods based upon changes in arrhythmia surgery techniques.
The first epoch consisted of simple isthmus cryoablation, a strategy abandoned after nine patients.
The next 51 had right atrial maze procedures for right atrial reentry tachycardia.
The most recent 51 patients—those treated since 2003—have routinely received the more elaborate biatrial Cox maze-III procedure, which incorporates cryoablation of the left atrium. This change occurred in response to a shift in the predominant presenting arrhythmia from right atrial reentry tachycardia to more challenging cases of atrial fibrillation.
The classic Cox maze-III was supplemented with one additional cryoablation lesion running between the bases of the right and left atrial appendages and across the dome of the atria to reduce the incidence of postoperative atrial tachycardia.
There were one early and six late deaths among the 111 patients. Six patients required cardiac transplantation, with two of the six late deaths in the series coming 4 and 24 days post transplantation. The other four donor heart recipients are alive 5–7 years later.
With follow-up extending to 12 years, 88% of patients have experienced an improvement in New York Heart Association functional class. The arrhythmia recurrence rate was 13.5% overall, declining to just 8% in the most recent group comprised of 51 Cox maze-III-treated patients.
Postoperative arrhythmia recurrence in patients with preoperative refractory atrial fibrillation took the form of atrial tachycardia, Dr. Mavroudis continued, which is far more easily treated.
In a multivariate analysis, the strongest risk factor for death or transplantation was protein-losing enteropathy, present preoperatively in three patients and associated with an 87-fold increased risk.
A right or ambiguous ventricle and preoperative moderate to severe atrioventricular valve dysfunction also predicted poor outcome.
Discussant Dr. Joseph A. Dearani praised Dr. Mavroudis for heading what the congenital heart disease surgery community recognizes to be the world's premier Fontan conversion program.
“The most important contribution from their experience is the thorough understanding of the different atrial arrhythmias that occur in the failing Fontan circulation and their methods of ablation, which have evolved over time,” observed Dr. Dearani, a cardiothoracic surgeon at the Mayo Clinic, Rochester, Minn.
“The importance of the need to address both atria at the time of operation cannot be overemphasized,” he added.
Noting that the late deaths and cardiac transplantations in the Chicago series all occurred relatively early—within a year after Fontan conversion—Dr. Dearani asked whether it might make more sense to consider protein-losing enteropathy, significant atrioventricular valve regurgitation, and severe ventricular dysfunction to be contraindications to Fontan conversion and instead send affected patients directly to heart transplantation.
Dr. Mavroudis, however, answered that he would not yet include atrioventricular valve regurgitation as a contraindication. This is because his recent experience using Alfieri valvuloplasty has, so far, been very encouraging.
At 12 years follow-up, 88% of patients saw an improvement in New York Heart Association functional class. DR. MAVROUDIS

Cardiology News, Volume 5, Issue 4, Page 28 (April 2007)