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Cabale Vilarino M.B.,University of Habana | Sanchez Serrano D.,Institute Cardiologia y Cirugia Cardiovascular
Revista Cubana de Investigaciones Biomedicas | Year: 2016

Introduction: The benefits of strict lipid control have become evident in primary and secondary prevention studies. Objective: Determine whether there is an association between lipid control and the absence of adverse coronary events in a five-year period. Methods: A prospective observational study was conducted with 424 patients cared for at the Dyslipidemia Service of the Cardiology and Cardiovascular Surgery Institute. All patients underwent lipidograms, and the risk category was used as a basis to determine whether they had managed to control their lipid levels during follow-up. Odds ratios were estimated to determine risk by logistic regression, whereas the Kaplan-Meier test was used for event-free survival. The difference between the groups was determined with the Cox-Mantel test. Results: An association was found between lipid control and the absence of coronary events during follow-up (p = 0.02). The need for myocardial revascularization was more common in the non-control group (p = 0.03). No association was found between the values for each lipid variable and the risk for adverse events. A history of ischemic heart disease was the only factor that showed a relationship to the incidence of coronary events. Conclusions: Despite the fact that during follow-up there was a relationship between control of lipid levels and the absence of coronary events, no association was observed between the values for each lipoprotein and the occurrence of adverse coronary events. © 2016, Editorial Ciencias Medicas. All rights reserved.


Recently there has been an increase in the study of heart failure with preserved ejection fraction (HFpEF); it usually has a stiffness of ventricular chambers and pathophysiology different from heart failure with reduced ejection fraction (HFrEF); both are associated with high morbidity and mortality. HFpEF is associated with older age, hypertension, diabetes and obesity, all with an increased incidence in recent years, therefore it represents a health problem in the near future. In HFpEF, structural changes may not be found; symptoms and serum biomarkers are not specific, then the confirmation of a diastolic dysfunction would be useful for diagnosis. Heart failure mortality has decreased in recent years due to the use of a number of drugs and procedures. Angiotensin receptor-neprilysin inhibitors have recently been introduced, which increase the prognosis of patients with HFrEF; however, no evidence exists of such decreased mortality in HFpEF. HFrEF patients show severe intolerance to exercise, associated with a decrease in peak oxygen consumption and quality of life. It has been found that exercise training improves all these issues by increasing cardiac output and yielding favorable peripheral responses; however there is only limited evidence that these effects also occur in HFpEF. New studies are required to prove that modern techniques of cardiac rehabilitation with exercise training also produce beneficial effects in patients with HFpEF. © 2015, Federacion Argentina de Cardiologia. All rights reserved.


Heres-Alvarez F.C.,Institute Cardiologia y Cirugia Cardiovascular | Peix-Gonzalez A.,Institute Cardiologia y Cirugia Cardiovascular
Revista Espanola de Cardiologia Suplementos | Year: 2011

C-reactive protein, an acute-phase reactant that plays a role in the innate immune response, has emerged as a prognostic biomarker for cardiovascular events in apparently healthy individuals and for event recurrence in patients with established coronary artery disease. Its possible usefulness not only for prognosis, but also as a therapeutic target, has made C-reactive protein the most thoroughly investigated inflammatory marker during the last 10 years. This paper describes some features of the relationship between C-reactive protein and coronary artery disease. It also discusses lifestyle and pharmacological interventions, particularly the use of statins, that may be associated with lower levels of this biomarker. These factors have contributed to the current view that C-reactive protein may serve as an indicator of responses to therapies intended for use in the primary and secondary prevention of coronary artery disease. © 2011 Sociedad Española de Cardiología. Publicado por Elsevier España, SL. Todos los derechos reservados.


Rivas-Estany E.,Institute Cardiologia y Cirugia Cardiovascular
Revista Espanola de Cardiologia Suplementos | Year: 2011

Numerous publications have highlighted the importance of physical exercise in the primary and secondary prevention of ischemic heart disease. Moreover, when used as part of a program of cardiac rehabilitation, physical training has also been reported to have a positive effect on quality of life and morbidity and mortality in patients with coronary artery disease and other cardiovascular conditions. These beneficial effects can only be obtained by complying with the basic principles of physical training, of which exercise intensity is an essential component. At present, it is generally believed that maintaining and promoting cardiovascular health requires aerobic exercise to be performed at a moderate intensity for at least 30 minutes 5 days a week or at a vigorous intensity for 20 minutes three times a week. Isometric exercise or resistance training should be considered even for patients with heart failure provided they are carefully selected and supervised. © 2011 Sociedad Española de Cardiología. Publicado por Elsevier España, SL. Todos los derechos reservados.


Molina R.Z.,Institute Cardiologia y Cirugia Cardiovascular
Revista Cubana de Investigaciones Biomedicas | Year: 2012

The congenital long QT syndrome is characterized by a prolongation of the QT interval and T wave abnormalities on the ECG, associated to a predisposition for the appearance of malignant ventricular arrhythmias (torsade de pointes), syncope, ventricular fibrillation and sudden cardiac death (SCD). Training in taking the measurements, penetrance and mutation variability, overlaps, mixed forms and overlap syndrome may all hamper diagnostic and therapeutic management. The present review intends to update essential aspects related to the diagnosis, genetic bases, physiopathological and molecular mechanisms, and therapeutic management of this complex channelopathy.


Alvarez-Collazo J.,Institute Cardiologia y Cirugia Cardiovascular | Diaz-Garcia C.M.,Institute Cardiologia y Cirugia Cardiovascular | Lopez-Medina A.I.,Institute Cardiologia y Cirugia Cardiovascular | Vassort G.,French Institute of Health and Medical Research | Alvarez J.L.,Institute Cardiologia y Cirugia Cardiovascular
Pflugers Archiv European Journal of Physiology | Year: 2012

Zinc exists in biological systems as bound and histochemically reactive free Zn2+ in the nanomolar range. Zinc is required as either structural or catalytic component for a large number of enzymes. It also modulates current passage through many ion channels. Here, we reinvestigated the effects of extracellular and intracellular Zn2+ on the Ltype Ca 2+ current (ICaL) and its modulation by β-adrenergic stimulation in rat ventricular cardiomyocytes. In the absence of Ca2+ ions, Zn2+ could permeate through the L-type channel at much lower concentrations and at a more positive voltage range, but with a lower permeability than Ca2+. In the presence of Ca2+, extracellular Zn2+ demonstrated strong bimodal inhibitory effects on the ICaL, with half-inhibition occurring around 30 nM, i.e., in the range of concentrations found in the plasma. Intracellular Zn2+ also significantly inhibited the ICaL with a half-inhibitory effect at 12.7 nM. Moreover, β-adrenergic stimulation was markedly reduced by intracellular Zn2+ at even lower concentrations (<1 nM) as a consequence of Zn2+-induced inhibition of the adenylyl cyclase. All these effects appeared independent of redox variations and were not affected by dithiothreitol. Thus, both basal intracellular and extracellular Zn2+ modulate transmembrane Ca2+ movements and their regulation by β- adrenergic stimulation. Considering that, in many pathological situations, including diabetes, the extracellular Zn2+ concentration is reduced and the intracellular one is increased, our results help to explain both Ca2+ overload and marked reduction in the β-adrenergic stimulation in these diseases. © 2012 Springer-Verlag Berlin Heidelberg.


Mustelier J.V.,Institute Cardiologia y Cirugia Cardiovascular
Revista Argentina de Cardiologia | Year: 2010

Background Percutaneous mitral valvuloplasty is currently the treatment of choice in patients with rheumatic mitral stenosis with suitable valvular anatomy. After the procedure, the development of severe mitral regurgitation is still a challenge. Objective To determine the causes of severe mitral regurgitation after percutaneous mitral valvuloplasty. Material and Methods A total of 110 percutaneous mitral valvuloplasties were consecutively performed in 107 patients (3 procedures were repeated due to restenosis) at the Instituto de Cardiología y Cirugía Cardiovascular in Cuba between June 17, 1998 and June 30, 2004 (106 using the Inoue technique and 4 with the Multi-Track system). The average follow-up was 24.6 months (maximum 72 and minimum 1.93 months). The severity of mitral regurgitation was evaluated according to the regurgitant jet area measured by Doppler echocardiography: Mild regurgitation when the area was <4 cm2, moderate when the area ranged from 4-8 cm2, and severe when it was >8 cm2. Left ventriculography was also used to quantify the severity of mitral regurgitation using Seller's criteria. The calibration of Doppler echocardiographic measures of the degree of mitral regurgitation (3 degrees of severity) by angiographic grading (4 degrees) provided the following grading ranges: 1+, mild regurgitation; 2+ and 3+, moderate regurgitation; and 4+, severe regurgitation. Results A total of five severe mitral regurgitations developed after the procedure (4.54%). A mitral valve replacement was necessary in three of them due to rupture of the anterior valve. The remaining two cases are still under medical treatment. Conclusion Multifactorial mechanisms are responsible for the development of mitral regurgitation after percutaneous mitral valvuloplasty, which may occur even in expert hands.


Castro Hevia J.A.,Institute Cardiologia y Cirugia Cardiovascular
Revista Cubana de Investigaciones Biomedicas | Year: 2012

The Brugada syndrome is a channelopathy causing between 4-12% of all sudden cardiac deaths and 20% in subjects with a "healthy heart". It is a clinical and electrocardiographic syndrome characterized by a convex electrocardiographic pattern in at least 2 right precordial leads as well a propensity to the occurrence of syncopes and/or cardiac arrest caused by polymorphic ventricular tachycardia and/or ventricular fibrillation. Malignant ventricular arrhythmias are caused by the transmural dispersion of repolarization and/or delayed conduction in the right ventricular outflow tract. It is more common in the male sex, frequently appearing in mid life. The risk of new events in symptomatic subjects is 30-40% in the 3 years following diagnosis. The treatment of choice is implantation of an automatic defibrillator. Quinidine has been used in patients with implanted defibrillators and frequent events of ventricular arrhythmia, as well as in those refusing to have such devices implanted. Management of asymptomatic subjects is under discussion. The database at the cardiac arrhythmia service of the Institute of Cardiology contains data for more than 80 patients with this syndrome, 45 with implanted automatic defibrillators.


Sanchez Dr. M.D.,Institute Cardiologia y Cirugia Cardiovascular
Revista Cubana de Investigaciones Biomedicas | Year: 2012

An overview is presented of the current status of cardiac ion channel diseases, their common characteristics and some distinguishing features. Ion channelopathies are inherited arrhythmogenic syndromes caused by ion channel traffic dysfunctions at membrane level (mutations in protein-encoding genes with gain or loss of function), life-threatening arrhythmias, syncope and sudden death, without any gross structural abnormality detectable by conventional methods. The past two decades have witnessed speedy progress in the understanding, diagnosis and treatment of these diseases, a situation which will continue to be as promising in the future with the application of molecular genetics. They are exclusion diagnoses. Structural heart diseases, electrolyte and metabolic disorders, other electrical causes and the use of antiarrhythmic drugs are all discarded. They appear in seemingly healthy young persons, whose debut may be a malignant ventricular arrhythmia or a sudden death event, from which only 5% are reanimated. They have a very broad clinical spectrum, ranging from asymptomatic cases (electrical signs, no syndromes) to fatal cases. Their actual frequency is unknown, due to: death, erroneous diagnosis, and minimal, intermittent or hidden signs. New diseases are incorporated, some overlap and it is very difficult to stratify risk before the debut. International registries have been developed. The paper presents the data contained in the Cuban National Channelopathy Register for patients reanimated from sudden death events and followed up for 10 years.


Alvarez-Collazo J.,Institute Cardiologia y Cirugia Cardiovascular | Alonso-Carbajo L.,Institute Cardiologia y Cirugia Cardiovascular | Lopez-Medina A.I.,Institute Cardiologia y Cirugia Cardiovascular | Alpizar Y.A.,Institute Cardiologia y Cirugia Cardiovascular | And 7 more authors.
Pflügers Archiv : European journal of physiology | Year: 2014

Cinnamaldehyde (CA), a major component of cinnamon, is known to have important actions in the cardiovascular system, including vasorelaxation and decrease in blood pressure. Although CA-induced activation of the chemosensory cation channel TRPA1 seems to be involved in these phenomena, it has been shown that genetic ablation of Trpa1 is insufficient to abolish CA effects. Here, we confirm that CA relaxes rat aortic rings and report that it has negative inotropic and chronotropic effects on isolated mouse hearts. Considering the major role of L-type Ca(2+) channels in the control of the vascular tone and cardiac contraction, we used whole-cell patch-clamp to test whether CA affects L-type Ca(2+) currents in mouse ventricular cardiomyocytes (VCM, with Ca(2+) as charge carrier) and in mesenteric artery smooth muscle cells (VSMC, with Ba(2+) as charge carrier). We found that CA inhibited L-type currents in both cell types in a concentration-dependent manner, with little voltage-dependent effects. However, CA was more potent in VCM than in VSMC and caused opposite effects on the rate of inactivation. We found these divergences to be at least in part due to the use of different charge carriers. We conclude that CA inhibits L-type Ca(2+) channels and that this effect may contribute to its vasorelaxing action. Importantly, our results demonstrate that TRPA1 is not a specific target of CA and indicate that the inhibition of voltage-gated Ca(2+) channels should be taken into account when using CA to probe the pathophysiological roles of TRPA1.

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