Ischemic Arrhythmias Research Articles

Susceptibility to ischemia-induced ventricular fibrillation in isolated female rat hearts varies moderately with estrous cycle stage

IntroductionThe vast majority of studies employing the isolated perfused rat heart model to study ischemic arrhythmias have used male rats only. The objective of this study was to determine the susceptibility to ischemia-induced ventricular fibrillation (VF) in isolated female rat hearts in each stage of the estrous cycle that corresponds with a different endogenous reproductive hormonal environment. MethodsHearts were isolated from female rats under pentobarbital anesthesia and perfused with modified Krebs solution containing 3mM K+. Experiments were grouped according to estrous cycle stage that was determined by prior vaginal lavage (n=10–13 per group). A group of male rat hearts was used as the control. Regional ischemia was induced by coronary ligation and maintained for 30min. The incidence of VF was determined from the ECG. ResultsThe incidence of VF in male hearts was 100%, while the incidence of VF in female hearts was also high but varied moderately with stage of the estrous cycle (diestrus 70%, metestrus 100%, proestrus 90%, estrus 69%; P>0.05). Compared to male hearts, the onset of VF was similar in all groups except for hearts excised from rats in proestrus, in which it was delayed. There was no difference between groups in an arrhythmia score, ischemic zone size, or baseline electrocardiographic or hemodynamic variables. DiscussionIn conclusion, the susceptibility of isolated female rat hearts to ischemic VF is comparable to that of male rat hearts, meaning that isolated female rat hearts can be used as controls in studies to assess antiarrhythmic drug efficacy. Since female rats can be used for isolated heart studies of ischemic VF, the need to cull female rats is reduced. However, the variation in VF susceptibility in female rat hearts that is associated with the different stages of the estrous cycle may affect statistical power that could potentially lead to Type II statistical errors. This problem can be prevented with careful randomization.

Ranolazine: Clinical Applications and Therapeutic Basis

Ranolazine is currently approved for use in chronic angina. The basis for this use is likely related to inhibition of late sodium channels with resultant beneficial downstream effects. Randomized clinical trials have demonstrated an improvement in exercise capacity and reduction in angina episodes with ranolazine. This therapeutic benefit occurs without the hemodynamic effects seen with the conventional antianginal agents. The inhibition of late sodium channels as well as other ion currents has a central role in the potential use of ranolazine in ischemic heart disease, arrhythmias, and heart failure. Despite its QTc-prolonging action, albeit minimal, clinical data have not shown a predisposition to torsades de pointes, and the medication has shown a reasonable safety profile even in those with structural heart disease. In this article we present the experimental and clinical data that support its current therapeutic role, and provide insight into potential future clinical applications.

Beneficial effects of hyperosmotic perfusion in the myocardium after ischemia/reperfusion injury in isolated rat hearts

A simple method to reduce the ischemia/reperfusion injury that can accompany cardiac surgery would have great clinical value. This study was to investigate the effect of hyperosmotic perfusion on ischemia/reperfusion injury in isolated perfused rat hearts. Forty male Sprague-Dawley rats were randomly divided either to have their isolated hearts perfused with normal osmotic buffer or buffer made hyperosmotic by addition of glucose. Hearts were then subjected to 30 min ischemia followed by 30 min reperfusion. Coronary flow, time to ischemic arrest, reperfusion arrhythmia, and ventricular function were recorded. Creatine phosphokinase leakage into the coronary artery, and myocardial content and activity of superoxide dismutase and catalase were also examined. Rat hearts with hyperosmotic perfusion showed higher coronary flow, a prolonged time to ischemic arrest (10.60 vs. 5.63 min, P<0.005), a lower reperfusion arrthythmia score (3.2 vs. 5.3, P<0.001), better ventricular function, and less creatine phosphokinase leakage (340.1 vs. 861.9, P<0.001) than normal osmotic controls. Myocardial catalase content and activity were increased significantly (1435 vs. 917 U/g wet weight, P<0.001) in hearts perfused with hyperosmotic solution in comparison to the normal osmotic controls. Pretreatment with hyperosmotic perfusion in normal rat hearts, which is attributed partly to the increased antioxidative activity, could provide beneficial effects from ischemia and reperfusion-induced injury by increasing coronary flow, and decreasing reperfusion arrhythmia.

Overexpression of microRNA-1 Causes Atrioventricular Block in Rodents

The present study was designed to investigate whether microRNAs (miRNAs) are involved in atrioventricular block (AVB) in the setting of myocardial ischemia (MI). A cardiac-specific miR-1 transgenic (Tg) mouse model was successfully established for the first time in this study using microinjection. miR-1 level was measured by real-time qRT-PCR. Whole-cell patch clamp was employed to record L-type calcium current (ICa,L) and inward rectifier K+ current (IK1). Expression of connexin 43 (Cx43) protein was determined by western blot analysis. Alternations of [Ca2+]i was detected by laser scanning confocal microscopy in ventricular myocytes. The incidence of AVB was higher in miR-1 Tg mice than that in wild-type (WT) mice. The normalized peak current amplitude of ICa,L was lower in ventricular myocytes from miR-1 Tg mice as compared with WT mice. Similarly, the current density of IK1 was decreased in miR-1 Tg mice than that in WT mice. Compared with WT mice, miR-1 Tg mice exhibited a significant decrease of the systolic [Ca2+]i in ventricular myocytes but a prominent increase of the resting [Ca2+]i. Moreover, Cx43 protein was downregulated in miR-1 Tg mice compared to that in WT mice. Administration of LNA-modified antimiR-1 reversed all the above changes. miR-1 overexpression may contribute to the increased susceptibility of the heart to AVB, which provides us novel insights into the molecular mechanisms underlying ischemic cardiac arrhythmias.

Ginkgo biloba Extract and Ginkgolide Antiarrhythmic Potential by Targeting hERG and ICa-L Channel

We investigated the effects of Ginkgo biloba extract (GBE) and ginkgolide (GLD) on human ether-a-go-go-related gene (hERG)-encoded K+ channels and its underlying mechanisms in the hERG-HEK293 cell line by determining GBE- and GLD-induced changes in action potential duration (APD), L-type calcium currents (ICa-L), and the intracellular calcium concentration ([Ca2+]i) in guinea-pig ventricular myocytes. hERG currents, APD and ICa-L were recorded using the whole-cell patch clamp technique, the [Ca2+]i was examined by an immunofluorescence experiment. In the present study, we found that a low concentration of GBE (0.005 mg/ml) increased hERG currents, but the high concentration of GBE (from 0.05 to 0.25 mg/ml) reduced hERG currents. GLD reduced hERG currents in a concentration-dependent manner (from 0.005 to 0.25 mg/ml). Both GBE and GLD altered kinetics of the hERG channel. GBE accelerated the activation of hERG channels without changing the inactivation curve, but reduced the time constant of inactivation; GLD did not shift the activation or the inactivation curve, but only reduced the time constant of inactivation. Both GBE and GLD shortened the APD, inhibited the ICa-L currents, and decreased the [Ca2+]i in isolated guinea-pig ventricular myocytes. The results indicate that GBE and GLD can prevent ischemic arrhythmias and have an antiarrhythmic effect potential via inhibition of IKr and ICa-L currents.

Mesenchymal stem cell therapy in heart disease

Cardiovascular disease is among the main causes of mortality and morbidity worldwide. Despite significant advances in medical and interventional therapy, the prognosis of conditions such as ischemic heart disease is still dismal. There is thus a need to investigate new therapeutic tools, one of which is stem cell therapy. Hematopoietic stem cells are the most studied type, and the fact that their biology is relatively well understood has led to their being used in preclinical research and clinical trials. However, the results of some of these studies have been controversial, which has opened the way for studies on other cell types, such as mesenchymal stem cells. These cells have immunomodulatory properties which suggest that they have therapeutic potential in cardiology. In the present article, the authors review the state of the art regarding mesenchymal stem cells, from basic and translational research to their use in clinical trials on ischemic heart disease, heart failure and arrhythmias, and discuss possible future uses.

A Clinical Approach to a Family History of Sudden Death

Sir William Osler reportedly once said, “Varicose veins are the result of an improper selection of grandparents.” Indeed, our family history strongly influences many aspects of our cardiovascular system, with the magnitude of effect ranging from very strong for autosomal dominant genetic disorders to more subtle in the setting of complex multigenic diseases like coronary atherosclerosis and hypertension. Accordingly, the standard evaluation of any new patient who presents to a physician includes assessment of their family history. Unfortunately, the family history may sometimes be discounted as noncontributory without detailed review. This can be exacerbated by busy office schedules with declining amounts of time available for comprehensive evaluations. A few minutes saved might seem to justify the lack of focus on an aspect of history that is sometimes deemed not to be particularly useful. However, a thorough assessment of family history also may provide the key diagnostic information to determine the cause of an illness, to determine who else is at risk of disease within the family, to add useful prognostic information, and to help for family planning and reproductive decisions. A family history of sudden death should prompt consideration of a wide range of heritable cardiovascular conditions, including many monogenic disorders (Table). However, the terms used by the lay public to describe sudden death may not adequately explain the cause of death on initial consideration. For instance, the phrase “heart attack” may be used to describe sudden death of any etiology. Further questioning may help one to discern whether there was a history of heart failure, cardiomyopathy, coronary artery disease (or its risk factors), aortic aneurysm, or features of syndromic disorders that are associated with sudden death. View this table: Table. Monogenic Disorders Associated With Sudden Death A 40-year-old man presents to a physician for evaluation of palpitations. These occur briefly about once per …

Terapia celular cardíaca com células mesenquimatosas

Cardiovascular disease is among the main causes of mortality and morbidity worldwide. Despite significant advances in medical and interventional therapy, the prognosis of conditions such as ischemic heart disease is still dismal. There is thus a need to investigate new therapeutic tools, one of which is stem cell therapy. Hematopoietic stem cells are the most studied type, and the fact that their biology is relatively well understood has led to their being used in preclinical research and clinical trials. However, the results of some of these studies have been controversial, which has opened the way for studies on other cell types, such as mesenchymal stem cells. These cells have immunomodulatory properties which suggest that they have therapeutic potential in cardiology. In the present article, the authors review the state of the art regarding mesenchymal stem cells, from basic and translational research to their use in clinical trials on ischemic heart disease, heart failure and arrhythmias, and discuss possible future uses.

Protective effects of dexrazoxane against acute ischaemia/reperfusion injury of rat hearts

Dexrazoxane (DEX), an inhibitor of topoisomerase II and intracellular iron chelator, is believed to reduce the formation of reactive oxygen species (ROS) and protects the heart from the toxicity of anthracycline antineoplastics. As ROS also play a role in the pathogenesis of cardiac ischaemia/reperfusion (I/R) injury, the aim was to find out whether DEX can improve cardiac ischaemic tolerance. DEX in a dose of 50, 150, or 450 mg·(kg body mass)(-1) was administered intravenously to rats 60 min before ischaemia. Myocardial infarct size and ventricular arrhythmias were assessed in anaesthetized open-chest animals subjected to 20 min coronary artery occlusion and 3 h reperfusion. Arrhythmias induced by I/R were also assessed in isolated perfused hearts. Only the highest dose of DEX significantly reduced infarct size from 53.9% ± 4.7% of the area at risk in controls to 37.5% ± 4.3% without affecting the myocardial markers of oxidative stress. On the other hand, the significant protective effect against reperfusion arrhythmias occurred only in perfused hearts with the dose of DEX of 150 mg·kg(-1), which also tended to limit the incidence of ischaemic arrhythmias. It is concluded that DEX in a narrow dose range can suppress arrhythmias in isolated hearts subjected to I/R, while a higher dose is needed to limit myocardial infarct size in open-chest rats.

Analysis of population appealability for emergent medical care for cardiac reasons

Aim. To study the structure of appealability of the population for emergency medical care for cardiac reasons, and the conformity between the cardiac cause and diagnosis. Methods. Analyzed was the statistical data of appealability of the population for emergency medical care for cardiac reasons in a large industrial center of the Republic of Tatarstan, city of Kazan. Register cards of ambulance calls for the year 2010 served as materials for the study. Results. It was established that cardiac reasons account for 30% of all adult requests for emergency medical care. The main flow (96.4%) was formed by the primary appeals to the ambulance station, and much less frequently (3.6%) by primarily detectable visits to health institutions for acute forms of ischemic heart disease and arrhythmias. Analyzing the structure of cardiac reasons in nature of the requests for care it was revealed that the proportion of disease with a sudden cardiac profile is 37.1%, with acute care of different profiles - 44.5%, sudden illness of other profiles - 16.5%, other - 1.9%. The proportion of disease with a sudden cardiac profile in the structure of other reasons for seaking medical care is 5.5%. During primary referral to the ambulance station the frequency of diseases with a sudden cardiac profile varies depending on the reason and ranges from 24 to 38.9%. Conclusion. These established features of the analysis of appealability of the population for emergent medical care for cardiac reasons provides the basis for the establishment and improvement of the algorithm of questions to ask the caller of an ambulance and its introduction into the work of the dispatching service, which will increase the frequency of conformity of the cause and diagnosis.

Vagal nerve modulation: A promising new therapeutic approach for cardiovascular diseases

The physiological activities of the mammalian heart are regulated by the autonomic nervous system. An imbalanced autonomic nervous system with increased sympathetic tone and reduced vagal tone has been implicated in cardiovascular diseases. Experimental and clinical reports have demonstrated that vagal nerve activation is able to improve outcomes for multiple cardiovascular diseases, such as ischaemic heart disease, heart failure, arrhythmia and hypertension. In this paper, we mainly focus on the potential cardioprotective mechanisms of vagal nerve activation. Based on the knowledge gained from our experiments and other published reports, vagal activation results in cardioprotection is not only associated with heart rate, anti-adrenergic effect but also related to anti-inflammatory activity, regulation of cellular redox states and regulation of mitochondrial targets. In conclusion, vagal nerve activation may be a promising new therapeutic approach for the treatment of cardiovascular diseases.

Aldehyde Dehydrogenase Type 2 Activation by Adenosine and Histamine Inhibits Ischemic Norepinephrine Release in Cardiac Sympathetic Neurons: Mediation by Protein Kinase Cε

During myocardial ischemia/reperfusion, lipid peroxidation leads to the formation of toxic aldehydes that contribute to ischemic dysfunction. Mitochondrial aldehyde dehydrogenase type 2 (ALDH2) alleviates ischemic heart damage and reperfusion arrhythmias via aldehyde detoxification. Because excessive norepinephrine release in the heart is a pivotal arrhythmogenic mechanism, we hypothesized that neuronal ALDH2 activation might diminish ischemic norepinephrine release. Incubation of cardiac sympathetic nerve endings with acetaldehyde, at concentrations achieved in myocardial ischemia, caused a concentration-dependent increase in norepinephrine release. A major increase in norepinephrine release also occurred when sympathetic nerve endings were incubated in hypoxic conditions. ALDH2 activation substantially reduced acetaldehyde- and hypoxia-induced norepinephrine release, an action prevented by inhibition of ALDH2 or protein kinase Cε (PKCε). Selective activation of G(i/o)-coupled adenosine A(1), A(3), or histamine H(3) receptors markedly inhibited both acetaldehyde- and hypoxia-induced norepinephrine release. These effects were also abolished by PKCε and/or ALDH2 inhibition. Moreover, A(1)-, A(3)-, or H(3)-receptor activation increased ALDH2 activity in a sympathetic neuron model (differentiated PC12 cells stably transfected with H(3) receptors). This action was prevented by the inhibition of PKCε and ALDH2. Our findings suggest the existence in sympathetic neurons of a protective pathway initiated by A(1)-, A(3)-, and H(3)-receptor activation by adenosine and histamine released in close proximity of these terminals. This pathway comprises the sequential activation of PKCε and ALDH2, culminating in aldehyde detoxification and inhibition of hypoxic norepinephrine release. Thus, pharmacological activation of PKCε and ALDH2 in cardiac sympathetic nerves may have significant protective effects by alleviating norepinephrine-induced life-threatening arrhythmias that characterize myocardial ischemia/reperfusion.

Carvedilol suppresses fatty acid oxidation and stimulates glycolysis in C2C12 cells

Beta adrenergic receptor blocking drugs (β-blockers) are used chronically in many cardiovascular diseases such as hypertension, ischemic heart disease, arrhythmia, and heart failure. Beneficial effects are associated with the inhibition of symphathetic nervous system hyperactivity, reduction of heart rate, and remodeling by blocking the mitogenic activity of catecholamines. A possible effect of β-blockers on substrate metabolism has also been suggested. The direct effects of β-blockers on mouse C2C12 cells were investigated in this study. C2C12 cells were grown in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and differentiated into myotubes in the same medium that contained 1% FBS. Palmitic acid oxidation and glycolysis were measured by using [9,10-(3)H]palmitate and [5-(3)H]glucose, respectively. The amount of (3)H(2)O was measured as an indicator of substrate usage. Carvedilol (100 µmol/L) inhibited palmitate oxidation and increased glycolysis by nearly 50%. Prazosin altered substrate metabolism in a similar fashion as carvedilol, whereas propranolol or bisoprolol were devoid of metabolic effects. When added to mimic sympathetic activation, epinephrine stimulated glycolysis but did not alter fatty acid oxidation. Based on these results, carvedilol appears to have direct effects on substrate metabolism that are related to the blockade of α1 adrenergic receptors.

The anti-infarct, antistunning and antiarrhythmic effects of oleuropein in isolated rat heart.

Previous studies have reported that oleuropein, the major constituent of olive leaves, has cardioprotective effects. There is no report related to oleuropein and ischemic-reperfusion injuries (cardiac dysfunction and myocardial infarction) as well as preconditioning in rat hearts. 56 male Wistar rats were divided into 7 groups (n=8). Group 1 as the control group and groups 2 to 7 as the treatment groups that received a single dose of oleuropein (100 mg/kg, i.p.) 1, 3, 6, 12, 24 and 48 hours before the excision of the heart, respectively. After these times, their hearts were excised and subjected to 30 min regional ischemia and 120 min reperfusion under Langendorff apparatus. Electrocardiogram and intraventricular pressures were monitored and recorded throughout the procedure. Finally, infarct size was measured by triphenyltetrazolium chloride staining. Compared to the control group, oleuropein significantly reduced infarct size and reperfusion-induced cardiac dysfunction in groups 2 and 3. Oleuropein markedly attenuated both ischemic and reperfusion arrhythmias in groups 2 and 3. There was no significant difference between other groups (4 to 7) than the control group. Heart rate had no significant difference among all of the groups. These results indicate that pretreatment of rats with a single dose of intraperitoneal oleuropein could protect their heart against ischemic-reperfusion injury for at least 3 hours. However, it has no preconditioning effect, since oleuropein had not cardioprotective effects 24 hour later.

Susceptibility of the isolated female rat heart to ischemia‐induced ventricular fibrillation varies with estrous cycle stage

The vast majority of studies employing the isolated perfused rat heart model to study ischemic arrhythmias have used male rats only. The objective of this study was to determine the variation in susceptibility to ischemia‐induced ventricular fibrillation (VF) in isolated female rat hearts with the changing endogenous reproductive hormonal environment associated with the estrous cycle.Hearts were isolated from female rats under anesthesia and perfused with 3 mM K+ Krebs solution. Experiments were grouped according to estrous cycle stage that was determined by prior vaginal lavage (n=9–13 per group). A group of male rats was used as the control. Regional ischemia was induced by coronary ligation and maintained for 30 min. The incidence of VF was determined from the ECG.The incidence of VF in male hearts was 100%, while the incidence of VF in female hearts was also high but varied with stage of the estrous cycle (proestrus 89%, diestrus 78%, metestrus 100%, estrus 69%; p&gt;0.05). There was no difference between groups in time to onset of VF or ischemic zone size (range 40–44% of total ventricular weight).In conclusion, the susceptibility of isolated female rat hearts to ischemic VF is comparable to that of male rat hearts. However, the variation in VF susceptibility in female rat hearts associated with the different stages of the estrous cycle may affect the statistical power of a study.Supported by a WVSOM intramural grant.

Prevalence of cardiovascular disease in subjects hospitalized due to chronic obstructive pulmonary disease in Beijing from 2000 to 2010

ObjectivesTo investigate the overall prevalence of cardiovascular disease (CVD) in subjects hospitalized for chronic obstructive pulmonary disease (COPD), and explore the prevalence of the major CVD complications and trends in patients with COPD over a 10-year period.MethodsMedical records in the PLA General Hospital, Beijing Union Medical College Hospital, and Beijing Hospital from 2000/01/01 to 2010/03/03 were retrospectively reviewed. A total of 4960 patients with COPD were reviewed in the study (3570 males, mean age, 72.2 ± 10.5 years; 1390 females, mean age, 72.0 ± 10.4 years).ResultsThe prevalence of CVD in COPD patients was 51.7%. The three most prevalent CVDs were ischemic heart disease (28.9%), heart failure (19.6%), and arrhythmia (12.6%). During the 10-year study period, the prevalence of various CVDs in COPD patients showed a gradual increasing trend with increasing age. There was higher morbidity due to ischemic heart disease (P < 0.01) in male COPD patients than in the female counterparts. However, heart failure (P < 0.01) and hypertension (P < 0.01) occurred less frequently in male COPD patients than in female COPD patients. Furthermore, the prevalence of ischemic heart disease decreased year by year. In addition to heart failure, various types of CVD complications in COPD patients tended to occur in younger subjects. The prevalence of all major types of CVD in women tended to increase year by year.ConclusionsThe prevalence of CVD in patients hospitalized for COPD in Beijing was high. Age, sex and CVD trends, as well as life style changes, should be considered when prevention and control strategies are formulated.

Antiarrhythmic effect of prolonged morphine exposure is accompanied by altered myocardial adenylyl cyclase signaling in rats

BackgroundMorphine is often administered to patients for pain management, but it is also recommended to ameliorate some types of cardiovascular diseases. Nevertheless, there is a lack of information regarding the effect of prolonged morphine treatment on myocardial adenylyl cyclase (AC) signaling, which plays an important role in regulating heart function. MethodsThe present work has investigated the consequences of 10-day administration of high morphine doses (10mg/kg per day) to adult Wistar rats for functioning of the G-protein-mediated AC signaling system. ResultsMorphine treatment appreciably affected neither the number of myocardial β-adrenoceptors nor the content of selected subunits of trimeric G-proteins (Gsα, Gi/oα, Gzα, Gq/11α and Gβ) but the amount of the dominant myocardial AC isoform V/VI almost doubled. These alterations were accompanied by a marked AC supersensitization: the enzyme activity stimulated by manganese, fluoride, forskolin or isoproterenol was considerably increased (by about 50–100%). In contrast, the ability of opioid agonists to inhibit forskolin-stimulated AC activity was slightly but significantly decreased in both groups. Besides that, morphine markedly decreased the incidence of ischemic ventricular arrhythmias induced by coronary artery occlusion, but did not significantly influence infarct size and arrhythmias occurring during reperfusion. ConclusionsOverall, these results indicate that prolonged treatment of rats with high doses of morphine substantially alters the function of myocardial G-protein-regulated AC signaling. These alterations are accompanied by a reduced susceptibility to ischemia-induced ventricular arrhythmias.

Effects of diurnal temperature range on cardiovascular and respiratory hospital admissions in Korea

The effects of heat and cold waves have been studied as risk factors for cardiovascular and respiratory diseases. However, few studies have examined the effect of diurnal temperature changes on health. We hypothesized that the diurnal temperature range (DTR) may affect the rate of hospital admissions for cardiovascular- and respiratory-related diseases, and therefore investigated the risk of hospital admissions of cardiovascular (stroke, myocardial infarction, ischemic heart disease, cardiac failure, cardiac disease, and arrhythmia) and respiratory (asthma, chronic obstructive pulmonary disease, and pneumonia) diseases attributable to DTR in four metropolitan areas in Korea during 2003–2006. The area-combined effects of DTR on some cardiovascular and respiratory diseases were significantly increased by an increment of DTR. In particular, the effects on cardiac failure and asthma were significant with the percentage change of hospital admissions per 1°C increment of DTR at 3.0% (95% CI, 1.4–4.6) and 1.1% (95% CI, 0.1–2.0), respectively, among 9 diseases. For those 75years and older, the DTR effect on asthma admissions was greater than in those aged under 75years. These results support the hypothesis of a positive association between DTR and cardiovascular and respiratory hospital admission.

Sexual Activity and Cardiovascular Disease

Sexual activity is an important component of patient and partner quality of life for men and women with cardiovascular disease (CVD), including many elderly patients.1 Decreased sexual activity and function are common in patients with CVD and are often interrelated to anxiety and depression.2,3 The intent of this American Heart Association Scientific Statement is to synthesize and summarize data relevant to sexual activity and heart disease in order to provide recommendations and foster physician and other healthcare professional communication with patients about sexual activity. Recommendations in this document are based on published studies, the Princeton Consensus Panel,4,5 the 36th Bethesda Conference,6–10 European Society of Cardiology recommendations on physical activity and sports participation for patients with CVD,11–13 practice guidelines from the American College of Cardiology/American Heart Association14–16 and other organizations,17 and the multidisciplinary expertise of the writing group. The classification of recommendations in this document are based on established ACCF/AHA criteria (Table). View this table: Table. Applying Classification of Recommendation and Level of Evidence Numerous studies have examined the cardiovascular and neuroendocrine response to sexual arousal and intercourse, with most assessing male physiological responses during heterosexual vaginal intercourse.18–24 During foreplay, systolic and diastolic systemic arterial blood pressure and heart rate increase mildly, with more modest increases occurring transiently during sexual arousal. The greatest increases occur during the 10 to 15 seconds of orgasm, with a rapid return to baseline systemic blood pressure and heart rate thereafter. Men and women have similar neuroendocrine, blood pressure, and heart rate responses to sexual activity.24,25 Studies conducted primarily in young married men showed that sexual activity with a person's usual partner is comparable to mild to moderate physical activity in the range of 3 to …

Actualización en cardiología geriátrica

This article contains a review of the main developments in the field of geriatric cardiology reported during 2011. The principle focus is on research into the characteristics of elderly patients with heart failure, arrhythmias (e.g. into atrial fibrillation and implantable cardioverter-defibrillators), ischemic heart disease and percutaneous interventions.