Relación entre rigidez arterial y factores de riesgo cardiovascular

To the Editor:

We read the article “Association of Arterial Stiffness With Obesity in Australian Women: A Pilot Study” by Pal and colleagues[1]with great interest. They investigated arterial stiffness in overweight/obese Australian women compared with their lean counterparts. They concluded that increased arterial stiffness existed in overweight patients compared with lean patients. In addition, arterial stiffness was positively associated with measurements of body composition, triglycerides and glucose levels, and systolic and diastolic blood pressures. They also concluded that arterial stiffness is associated with obesity, along with other metabolic abnormalities in obese Australian women. We congratulate the authors for this important study. However, we do not share the opinion that aortic stiffness can be affected definitely by cardiovascular risk factors such as smoking, alcohol consumption, and hypercholesterolemia.

Previous studies proposed that several cardiovascular risk factors might affect arterial stiffness, such as age, body weight, smoking, alcohol consumption, hypertension, cholesterol and triglyceride concentrations, and glucose levels.[2] Recently, Cecelja and colleagues[3] published a systematic review which showed that the contribution of cardiovascular risk factors other than age and blood pressure to aortic stiffness measured by carotid-femoral pulse wave velocity is small or insignificant. They demonstrated that age and blood pressure were consistently independently associated with aortic stiffness (91% and 90% of studies, respectively). Diabetes mellitus was associated with aortic stifness in 52% of studies, but the strength of the association was low. The majority of studies found no independent association between aortic stiffness and sex, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, smoking, and body mass index. This systematic review showed that only age and blood pressure were consistently independently associated with aortic stiffness in the majority of studies.[3]

Arterial stiffness describes the reduced capability of an artery to expand and contract in response to pressure changes and it is an independent predictor of cardiovascular morbidity and all-cause mortality.[4] It has been suggested that aortic stiffness occurs as a result of atherosclerosis along the aorta. However, there is little or no association between aortic stiffness and classical risk factors for atherosclerosis, other than age and blood pressure.[3]

It has also been shown that some antihypertensive drugs like angiotensin-converting enzyme inhibitors, calcium channel blockers and spiranolactone, and statins reduce aortic stiffness.[4] Pal and colleagues did not also mention these drugs, which might affect aortic stiffness, and would have been useful if they had provided information about these factors.

The results of the study might be specific to this obese Australian women patient group. In other words, there might be an association of cardiovascular risk factors with aortic stiffness in this group. These results cannot be generalized to the general population. Only age and blood pressure were consistently independently associated with aortic stiffness in the majority of previous studies.[3]

References

Pal S, Radavelli-Bagatini S. Association of arterial stiffness with obesity in Australian women: a pilot study. J Clin Hypertens (Greenwich). 2013;15:118–123. Albu A, Fodor D, Bondor C, et al. Arterial stiffness, carotid atherosclerosis and left ventricular diastolic dysfunction in postmenopausal women. Eur J Intern Med. 2013;24:250–254. Cecelja M, Chowienczyk P. Dissociation of aortic pulse wave velocity with risk factors for cardiovascular disease other than hypertension: a systematic review. Hypertension. 2009;54:1328–1336. Cavalcante JL, Lima JA, Redheuil A, Al-Mallah MH. Aortic stiffness: current understanding and future directions. J Am Coll Cardiol. 2011;57:1511–1522.

Cardiovascular Effects of Drugs Used to Treat Alzheimer's Disease

Drug Saf |  Cardiovascular Effects of Drugs Used to Treat Alzheimer's Disease; Howes L; Drug Safety (Apr 2014) Tags: Arrhythmias Dementia donepezil galantamine memantine rivastigmine

Drugs that are used to treat Alzheimer's disease include the acetyl cholinesterase inhibitors (ACHIs) donepezil, rivastigmine and galantamine and the NMDA receptor antagonist memantine. Adverse cardiovascular events with these drugs are very uncommon. However, there is evidence that ACHI therapy is associated with a small but significant increase in the risk of syncope and bradycardia. There are also a few reports that these drugs may occasionally be associated with QT prolongation and torsades de pointes ventricular tachycardia. Adverse cardiovascular effects of ACHIs including syncope and bradycardia are less common than their adverse gastrointestinal effects, but they remain important considerations in susceptible individuals. In contrast, animal studies and some observational studies suggest that ACHIs may reduce myocardial infarction and cardiovascular mortality and have favourable effects on hemodynamics and survival in heart failure. Further research is required to confirm these potential beneficial effects. Little is known about the cardiovascular effects of memantine but there have been reports of bradycardia and reduced cardiovascular survival associated with its use.

Riesgo de fibrilacion auricular y consumo de bebidas alcohólicas

Even in moderation, consumption of wine and hard liquor may be a risk factor for atrial fibrillation, an abnormally fast heartbeat that can lead to stroke, heart failure and dementia, according to new research published in the Journal of the American College of Cardiology. The research did not identify a similar risk for moderate consumption of beer.

Researchers in Sweden studied 79,016 adults, ages 45 to 83, who completed an extensive questionnaire about food and alcohol consumption in 1997. The researchers followed the participants for up to 12 years through national registries in Sweden and found 7,245 cases of atrial fibrillation.

Consistent with previous research, the study found an association between high alcohol consumption, defined as more than three drinks per day, and increased risk for atrial fibrillation and a strong association with binge drinking. Previous studies had not reported findings on moderate alcohol use.

The Swedish study showed an increase in risk for atrial fibrillation with moderate drinking of wine and liquor. Moderate drinking was defined as one to three drinks per day.

The researchers also conducted a complementary meta-analysis, combining their results with six similar prospective research studies to study the dose response. The complete analysis included 12,554 cases of atrial fibrillation. The meta-analysis, which didn't differentiate between types of alcohol, showed the risk for atrial fibrillation increased 8 percent with each additional drink per day.

While many studies have shown that light to moderate alcohol consumption can have beneficial outcomes on the heart, such as reducing ischemic heart disease and stroke, it is important to balance these benefits against the potential risk of developing atrial fibrillation, said Susanna C. Larsson, Ph.D., Associate Professor, Unit of Nutritional Epidemiology, Institute of Environmental Medicine at the Karolinska Institutet in Stockholm, and lead author of the study.

The study showed that binge drinking - consuming five or more drinks on a single occasion - was associated with an increased risk for drinkers of wine and liquor. Excluding binge drinkers from the analysis reduced the risk only slightly for heavy and moderate drinkers of wine and liquor.

While the association between moderate wine and liquor consumption and increased atrial fibrillation risk was strong, the Swedish study did not find such a relationship with atrial fibrillation and moderate beer consumption or even binge drinking of beer.

"We have no explanation for the lack of association with beer consumption," Larsson said. "It is likely that beer is consumed more regularly during the week, whereas wine and liquor is more often consumed during weekends only. Adverse effects of alcohol on atrial fibrillation risk may be less pronounced if alcohol consumption is spread out over the week compared with consumption of larger amounts of alcohol during a few days per week."

Prospective studies, which follow a group of participants over time, can identify associations, or conditions that exist together, but an association does not necessarily mean moderate alcohol use causes atrial fibrillation. There could be other reasons atrial fibrillation is seen more often in drinkers. Still investigators identified several factors that could explain the relationship between alcohol consumption and atrial fibrillation. Past studies have shown an association between alcohol consumption and depression of heart function, cardiac condition abnormalities, dilated cardiomyopathy with supraventricular arrhythmias and other conditions that could lead to atrial fibrillation.

Estatinas y probabilidad de originar enfermedad renal

Am J Cardiol. 2014 Jun 15;113(12):2018-20. doi: 10.1016/j.amjcard.2014.03.046. Epub 2014 Apr 3.
Statin and the risk of renal-related serious adverse events: Analysis from the IDEAL, TNT, CARDS, ASPEN, SPARCL, and other placebo-controlled trials.
Bangalore S1, Fayyad R2, Hovingh GK3, Laskey R2, Vogt L4, DeMicco DA2, Waters DD5; Treating to New Targets Steering Committee and Investigators.
Author information
Abstract
A recent study has shown an association between high-potency statins and risk of acute kidney injury. However, these data are from observational studies, and it is not clear if similar signal is seen from randomized controlled trials. We evaluated the risk of renal-associated serious adverse events (SAEs) using statins versus placebo trials and the high-dose versus low-dose statin trials that were available to us. The outcome of interest was renal-related SAEs. The incidence of adverse events relating to kidney injury was determined through review of the adverse event database. The following outcomes were evaluated: (1) renal-related SAEs within 120 days of randomization (primary outcome), (2) renal-related SAEs after 120 days of randomization (secondary), and (3) drug discontinuation due to renal-related SAEs (secondary). There was no difference in the incidence of renal-related SAEs at 120 days (0.04% vs 0.10%, p = 0.162) between atorvastatin and placebo in the 24 placebo-controlled trials (10,345 patients on atorvastatin (10 to 80 mg/day) versus 8,945 patients on placebo) or in the high-dose versus low-dose statin trials including the Incremental Decrease in End Points Through Aggressive Lipid Lowering (IDEAL) study (0.05% vs 0.02%, p = 0.625) or the Treating to New Targets (TNT) trial (0.0% vs 0.04%, p = 0.500) trial. Results were similar for renal-related SAEs after 120 days (placebo controlled trials [0.38% vs 0.36%, p = 0.905], IDEAL trial [0.56% vs 0.65%, p = 0.683], or the TNT trial [0.76% vs 1.04%, p = 0.168]) and for drug withdrawal due to renal-related SAE (placebo controlled trials [0.05% vs 0.04%, p = 1.00], IDEAL trial [0.02% vs 0.0%, p = 0.499], or the TNT trial [0.08% vs 0.12%, p = 0.754]). In conclusion, the results from clinical trials with data from 149,882 patient-years of follow-up fail to show any increase in renal-related SAEs with statins compared with controls

Estáticas y probabilidad de originar enfermedad renal

Am J Cardiol. 2014 Jun 15;113(12):2018-20. doi: 10.1016/j.amjcard.2014.03.046. Epub 2014 Apr 3.
Statin and the risk of renal-related serious adverse events: Analysis from the IDEAL, TNT, CARDS, ASPEN, SPARCL, and other placebo-controlled trials.
Bangalore S1, Fayyad R2, Hovingh GK3, Laskey R2, Vogt L4, DeMicco DA2, Waters DD5; Treating to New Targets Steering Committee and Investigators.
Author information
Abstract
A recent study has shown an association between high-potency statins and risk of acute kidney injury. However, these data are from observational studies, and it is not clear if similar signal is seen from randomized controlled trials. We evaluated the risk of renal-associated serious adverse events (SAEs) using statins versus placebo trials and the high-dose versus low-dose statin trials that were available to us. The outcome of interest was renal-related SAEs. The incidence of adverse events relating to kidney injury was determined through review of the adverse event database. The following outcomes were evaluated: (1) renal-related SAEs within 120 days of randomization (primary outcome), (2) renal-related SAEs after 120 days of randomization (secondary), and (3) drug discontinuation due to renal-related SAEs (secondary). There was no difference in the incidence of renal-related SAEs at 120 days (0.04% vs 0.10%, p = 0.162) between atorvastatin and placebo in the 24 placebo-controlled trials (10,345 patients on atorvastatin (10 to 80 mg/day) versus 8,945 patients on placebo) or in the high-dose versus low-dose statin trials including the Incremental Decrease in End Points Through Aggressive Lipid Lowering (IDEAL) study (0.05% vs 0.02%, p = 0.625) or the Treating to New Targets (TNT) trial (0.0% vs 0.04%, p = 0.500) trial. Results were similar for renal-related SAEs after 120 days (placebo controlled trials [0.38% vs 0.36%, p = 0.905], IDEAL trial [0.56% vs 0.65%, p = 0.683], or the TNT trial [0.76% vs 1.04%, p = 0.168]) and for drug withdrawal due to renal-related SAE (placebo controlled trials [0.05% vs 0.04%, p = 1.00], IDEAL trial [0.02% vs 0.0%, p = 0.499], or the TNT trial [0.08% vs 0.12%, p = 0.754]). In conclusion, the results from clinical trials with data from 149,882 patient-years of follow-up fail to show any increase in renal-related SAEs with statins compared with controls