El ajo podría ayudar a tratar la presión arterial elevada en combinación con los medicamentos tradicionales, publicó hoy una publicación especializada.

Investigadores de la Universidad de Adelaida, en Australia, involucraron en el estudio a 50 pacientes en un ensayo para conocer si los suplementos del condimento podrían ayudar a personas con hipertensión.

Trabajos previos mostraron que los suplementos de ajo reducen el colesterol malo y la presión arterial alta en aquellas personas sin tratamiento contra la enfermedad.

En la más reciente pesquisa, los científicos australianos analizaron los efectos de cuatro cápsulas al día por 12 semanas de un suplemento conocido como ajo envejecido, difundió la publicación Maturitas.

Los suplementos de ajo habían estado asociados con efectos de baja presión arterial en enfermos sin tratamiento contra la hipertensión, indicó el autor principal del estudio, Karin Ried.

Según el experto, este ensayo es el primero en probar si el extracto de ajo envejecido como tratamiento adicional a las terapias contra la hipertensión, pueden ayudar a combatir este problema cuando se encuentra descontrolado.

Expertos que no intervinieron en el estudio sugieren que estos resultados deben ser confirmados.

(Fuente: PL)

La exposición a pequeñas ondas de radio en los riñones pueden ayudar a tratar la hipertensión arterial en personas que no responden a las terapias convencionales, difundió hoy la revista The Lancet.

Científicos australianos seleccionaron varios nervios en los riñones que desempeñan un papel clave en la regulación de la presión arterial.

Aunque este método aún se encuentra en fase de prueba podría ayudar a cientos de pacientes hipertensos, indicaron del Instituto IDI de Corazón y Diabetes en Melbourne.

Para aplicar este tratamiento, cuya efectividad y seguridad se encuentra en prueba, los científicos introducen un catéter a través de una arteria en la ingle.

El cateter se encuentra conectado a una máquina que genera ondas de radio conocida como energía de radiofrecuencia.

De esta forma, una corta explosión desde la máquina puede golpear pequeños nervios del riñón.

Los investigadores han aplicado este método en pacientes con presión arterial alta en varios centros de atención y encontraron que su condición mejoró.

Aunque la presión arterial no bajó a niveles normales si permitió reducir los riesgos a la salud asociados con la presión arterial alta.

(Fuente: PL)

We performed a per-protocol analysis of the Japanese Trial to Assess Optimal Systolic Blood Pressure in Elderly Hypertensive Patients (JATOS) to evaluate the optimal target blood pressure (BP) in elderly hypertensive patients. In JATOS, conducted in elderly (65–85 years) hypertensive patients treated with efonidipine hydrochloride, there were no differences between the strict-treatment group (systolic BP maintained at <140 mm Hg) and the mild-treatment group (systolic BP maintained at greater than or equal to140 mm Hg and <160 mm Hg) in the incidence of primary end points (cardiovascular disease and renal failure) for 2 years.

The present study analyzed data in subgroups of JATOS in which the average systolic BP was within the range of target values.

The average BP levels achieved in the strict-target BP achieved subgroup (n=1191) and the mild-target BP achieved subgroup (n=1531) were 132.3/74.0 mm Hg and 146.6/78.3 mm Hg, respectively.
The incidences of primary end points were similar between these subgroups (11.1/1000 patients per year and 13.2/1000 patients per year, respectively, P=0.502), and there were also no differences in the incidences of adverse events.
The incidences of cardiovascular events in patients who failed to achieve their respective treatment goals, on the other hand, were significantly higher than in patients who achieved them.
These results indicate that strict treatment for elderly hypertensive patients may have little effect in enhancing the suppression of the onset of cardiovascular events as compared with mild treatment, although patients who have difficulties in achieving treatment goals should be given more aggressive treatment as a high-risk population.

(Fuente: Hypertension Research (2010) 33, 1124–1128)

Primary aldosteronism (PA) is one of the common forms of curable hypertension. Recent views have suggested that PA is far from being relatively benign, as it was previously thought, but it is associated with a variety of cardiovascular and renal sequelae that reflect the capability of inappropriately elevated aldosterone to induce tissue damage over that induced by hypertension itself. The evidence supporting these views has been obtained from experiments conducted in hypertensive animal models and studies involving patients with PA. Preclinical studies have also indicated that aldosterone causes cardiovascular and renal tissue damage only in the context of inappropriate salt status. It has been suggested that untoward effects of high-salt intake are dependent on activation of mineralocorticoid receptors (MRs) that might result from increased oxidative stress and changes in the intracellular redox potential. Unilateral adrenalectomy or treatment with MR antagonists are the current options for treating an aldosterone-producing adenoma (APA) or idiopathic adrenal hyperplasia (IHA). Treatments are effective in correcting hypertension and hypokalemia, and currently available information on their capability to prevent cardiovascular events and deterioration of renal function indicates that surgery and medical treatment are equally beneficial in the long term.

(Fuente: American Journal of Hypertension 2010)

Por: Paul W. Armstrong, M.D.

The transformation of cardiac care over the past half century has been breathtaking to witness. In large part, this transformation is due to the advent of new drugs and devices, improved health care systems, and behavioral modifications such as smoking cessation. Four cardiac medicines developed before 1960 that survived the turn of the millennium are aspirin, digoxin, warfarin, and spironolactone. New competitors threaten the continued longevity of aspirin, the survival of digoxin depends on evidence of its ability to improve exercise tolerance and quality of life in patients with heart failure, and new pretenders for warfarin are here. Remarkably, after over 50 years, the aldosterone antagonism achieved by spironolactone (and more recently eplerenone) has earned an enduring role in the treatment of heart failure.1

When spironolactone was developed, it was a minor player complementing more powerful diuretics in achieving volume homeostasis. Our understanding of heart failure was then predominantly focused on hemodynamic perturbations. As long ago as 1960, the drug was found to protect rats against myocardial necrosis,2 yet this observation languished for decades. Subsequently, two parallel tracks of knowledge emerged, which are germane to a resurgence of interest in antagonizing aldosterone. The first track involves the complex adaptations affecting the failing and remodeled heart. Cardiac enlargement and increased sphericity are often accompanied by scarring and fibrosis. Neurohormonal activation and altered vascular compliance of coronary and peripheral blood vessels compound this unfavorable milieu.3 The second track concerns the pleiotropic effects of aldosterone antagonists. These include conservation of potassium and magnesium, the depletion of which potentiates ventricular arrhythmias and sudden death; inhibition of fibroblast proliferation and perivascular fibrosis, which are promoted by chronic hyperaldosteronism; and reversal of unfavorable coronary and renal vascular remodeling, which is modulated by endothelial-cell and baroreceptor dysfunction.3

These physiological observations now appear to have important clinical consequences. In the Randomized Aldactone Evaluation Study (RALES), Pitt and colleagues4 demonstrated that spironolactone therapy could significantly reduce rates of death and hospital readmission for worsening heart failure among patients with functional class III or IV heart failure. Four years after this seminal study, the same investigators conducted the Eplerenone Post–Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS),5 which showed that eplerenone, a selective aldosterone-receptor blocker, reduced morbidity and mortality among patients recovering from acute myocardial infarction with complicating left ventricular dysfunction. As a result of these convincing findings, aldosterone-receptor blockade has become part of recommended therapy in such patients.6

In this issue of the Journal, Zannad and colleagues7 complete an aldosterone-trial trilogy with their report on the Eplerenone in Mild Patients Hospitalization and Survival Study in Heart Failure (EMPHASIS-HF; ClinicalTrials.gov number, NCT00232180), which shows that eplerenone reduces the rate of death from cardiovascular causes or hospitalization for heart failure by approximately 37%, as compared with placebo, in patients with functional class II heart failure. Although this effect seems surprisingly large for a trial of mildly symptomatic patients, careful review of the baseline characteristics is instructive.

The majority of the study patients were heart disease veterans: one half had previously been hospitalized for heart failure and had a history of myocardial infarction; hypertension, atrial fibrillation, and diabetes were also common. The mean ejection fraction of 26% (nearly identical to that in the more severely symptomatic patients in RALES) is a cogent reminder of the discordance between functional class and left ventricular function. An additional feature marking the EMPHASIS-HF patients as high risk is that approximately one quarter had left bundle-branch block, and the overall mean QRS duration was 122 msec (with one quarter having a QRS duration >130 msec). Although the concomitant use of beta-blockers and angiotensin-converting–enzyme inhibitors was common, the infrequent use of implantable defibrillators or cardiac resynchronization therapy raises the question of whether eplerenone would have fared as impressively had a larger proportion of the study population received implantable electrical devices, in alignment with current guidelines.6 This points to the need for further investigation, given that even the trial participants receiving active therapy had a 1-year mortality rate of approximately 5.0%.

The effect on death from cardiovascular causes or hospitalization for heart failure translates into an impressively low number needed to treat: 19 patients. The number needed to treat to prevent one death is 51 patients, positioning this therapy in the front rank of therapeutic choices. The survival curves invite speculation about whether the effect of eplerenone on volume homeostasis came into play early, thereby affecting hospitalization for heart failure sooner, whereas structural changes such as favorable cardiac remodeling might have accounted for the more delayed reduction in mortality.

The EMPHASIS-HF investigators have added real value to the management of heart failure. Since spironolactone is available for pennies a day, one might reasonably ask whether the greater cost of eplerenone is warranted or whether it is reasonable to simply assume that the current findings also apply to spironolactone and reserve the newer, more expensive therapy for those few patients in whom the side effects of spironolactone are disabling. I believe this would be a reasonable tactic. It is now time to overcome undertreatment by ensuring that this form of therapy is incorporated into all heart-failure regimens.8 It is incumbent on the prescriber to perform appropriate monitoring of renal and electrolyte status, which can enhance the safety of such treatment.9

As one reflects on the EMPHASIS-HF results, the question arises: Do they open doors for investigating aldosterone antagonism in other cardiovascular diseases? The answer is, most emphatically, yes. In fact, studies of this therapy in patients with diastolic dysfunction and acute myocardial infarction are ongoing, and the results are eagerly awaited. A preventive approach in patients at high cardiovascular risk might even be on the horizon.10 Of the quartet of therapies that have served us well over the past half century, aldosterone antagonism seems most likely to be the last man standing.

[Fuente: This article was published on November 14, 2010, at NEJM.org].