Background: Macitentan significantly improves pulmonary hemodynamics and survival in patients with primary pulmonary hypertension (PPH). Its beneficial effect, however, may be blunted due to the adverse impacts such as anemia and peripheral edema. Pulmonary arterial hypertension (PAH) is a significant consequence of congenital heart disease (CHD). Its presence and severity are associated with increased morbidity and mortality. We tried to evaluate that the effectiveness of the macitentan in patients with late-onset pulmonary hypertension after atrial septal defect operation in our center.
Methods: The effect of a single dose of macitentan (10 mg) on pulmonary hemodynamics, functional capacity was examined in four patients with late-onset pulmonary hypertension after atrial septal defect operation.
Results: The macitentan significantly improved mean pulmonary artery pressure (MPAP), cardiac output (CO), tricuspid annular plane systolic excursion (TAPSE), right ventricle systolic wave(RVS’), 6-minute walking test and NT-proBNP levels compared with before treatment.
Conclusions: Macitentan can be used in patients with late-onset pulmonary hypertension after shunt operation especially atrial septal defect.
With the invention of the stethoscope, in the early 1800s, a better diagnosis of heart and lung disorders was opened up. Through the stethoscope's 200-year history, there has been a significant development of the stethoscopy from the use of the simple monaural earpiece to the binaural stethoscope, followed by the electronic stethoscope, which, together with other studies, has enabled a thorough diagnosis of these disorders. Here is a glimpse of this story.
The cross-border investigation
Far back in time, it has been clear that the function of the heart and lungs played an important role in maintaining life. By tapping with the finger (percussion) and putting the ear to the patient's chest (auscultation), it could hear sound from the body telling about the patient's condition, especially about the presence of fluid or air-filled organs. Auscultation is already described in the Corpus Hippocraticum, in the Diseases II section [1]. The doctor puts the ear to the chest of a patient with water sores, to hear the pain as a wine vinegar from the lungs - or the doctor grabs the patient about the shoulders, shakes him and places his ear to his chest to hear in which side his pleuritis is sitting. Since then, auscultation seems to have been partially forgotten, although it has probably been known by Ambroise Paré and William Harvey [2]. It was not until the late 1700s that it became an important diagnostic aid, just like the pulse clock and the medical thermometer [3 p. 277]. Here, Joseph Leopold Auenbrugger (1722-1809) is considered to be the father of the modern physical examination, which is based on percussion. Percussion he performed by knocking direcly on the thorax with the finger or cupped hands. His discovery of the percussion sounds from the chest during inhaling and exhaling originates from his work in 1760 at the Vienna Military Hospital [4]. In 1761, His little book on thoracic percussion revealing thoracic diseases appeared in 1761 [3p.271], which in 1808 was translated into French by the Parisian physician Jean Nicolas Corvisart des Marets (1755-1821). This contributed to the French doctors starting to use percussion and ausculation more routinely [5].
The limitation of simple auscultation was the fact that the sound was weak and incomplete and therefore there was a need for improved sound quality. In addition, the direct contact with the patient's body could seem insulting
Introduction: the perennial pandemic: There are serious challenges posed by the SARS-CoV-2 virus and COVID-19 as the disease. With the persistence of the pandemic over one and half year, it is being feared that the COVID-19 may have become the new reality associated with human existence world over and the mankind may have to live with it for years or even decades. Further, the grievous nature of the disease is evolving further with genomic changes in the virus in form of mutations and evolution of variants, with enhanced infectivity and probably virulence.
Acute and chronic phases of COVID-19: Epidemiologically, it is becoming clear that apart from the advanced age and pre-existing conditions, such as diabetes, cardiovascular, pulmonary, and renal diseases, certain constituent factors render some patients more vulnerable to more severe forms of the disease. These factors influence the COVID-19 manifestations, its course, and later the convalescence period as well as the newly defined ‘Long COVID phase. The substantial continuing morbidity after resolution of the infection indicates persisting multisystem effects of ‘Long Covid’.
Lung damage associated with COVID-19: COVID-19 is primarily a respiratory disease presenting with a broad spectrum of respiratory tract involvement ranging from mild upper airway affliction to progressive life-threatening viral pneumonia and respiratory failure. It affects the respiratory system in various ways across the spectrum of disease severity, depending on age, immune status, and comorbidities. The symptoms may be mild, such as cough, shortness of breath and fevers, to severe and critical disease, including respiratory failure, shock, cytokine crisis, and multi-organ failure.
Implications for the post-COVID care: Depending on the severity of respiratory inflammation and damage, as well as associated comorbidities, duration of injury and genetics, the progressive fibrosis leads to constriction and compression of lung tissues and damage to pulmonary microvasculature. Consequently, the COVID-19 patients with moderate/severe symptoms are likely to have a significant degree of long-term reduction in lung function. Depending on the severity of the disease, extensive and long-lasting damage to the lungs can occur, which may persist after resolution of the infection.
Managing the long COVID’s challenges: Given global scale of the pandemic, the healthcare needs for patients with sequelae of COVID-19, especially in those with lung affliction are bound to increase in the near future. The challenge can be tackled by harnessing the existing healthcare infrastructure, development of scalable healthcare models and integration across various disciplines with a combination of pharmacological and non-pharmacological modalities. Following clinical and investigational assessment, the therapeutic strategy should depend on the disease manifestations, extent of damage in lungs and other organs, and associated complications.
Despite the fact, that lung cancer is more common among older smoking men, however it may also develop among young women without a smoking anamnesis. We report here a history of a non-smoking woman, 40 years old, with a diagnosis of lung adenocarcinoma at IV stage. Despite the fact, the woman received three lines of palliative chemotherapy, the disease progressed. After the sample of the tumor was tested by genetic approach, ROS1 mutation was detected, and the patient was treated with a ROS1 inhibitor, Crizotinib. Sharp improvement was observed already after the first week of treatment. After one-month adenocarcinoma shrink, and specific supraclavicular lymph nodes disappeared. Unfortunately, due to problems with financing the treatment was stopped, after what the disease began to progress rapidly, and the patient died after a month due to brain metastasis. This case is noteworthy also because the patient was first diagnosed a thrombophilia with thrombi present in deep calf veins, left heart ventricle and lungs Adenocarcinoma was discovered occasionally when during video-assisted thoracoscopic surgery biopsy specimen was taken from suspicious mass in the lower lobe of the right lung. This story reminds us that lung carcinoma may start with a paraneoplastic syndrome, like thrombophilia as in this case and finding of adenocarcinoma of the lung in young, non-smoking persons is indicative for possible ROS1 gene mutation. In such cases early treatment with ROS1 protein-tyrosine kinase inhibitors should be started as soon as possible.
Introduction
In actual pharmacological therapy we can see that some drugs can be added to other medical instruments to improve their activity: in example we can see medicated stent for some coronary disease, or hormonal medical devices used in pregnancy prevention, but other example are known today. In example Carmustine wafer is delivered by delivery systems in some brain cancer and radioactive seed implants in prostatic cancer. Ocular intra vitreal implants for some macular degenerations (MABS or cortisones) other implants delivery systems drugs, naltrexone implant for opiate dependence. Other strategies imply carrier use to deliver the drugs in the site of action: In example MABS linked to radioactive isotopes in some relapse of severe Hodgkin disease but many other example we can see in therapy used today. So we can think that other chronic conditions can be treated using a combination of drugs with other instrument to improve the clinical outcomes. This to make possible that the ERLICH MUGIC BULLETS can act in the right site reducing the side effect. In example today we can see various medical interventional radiological strategy to treat in coronary and hearth disease with medicate stents positioning or to local use of contrast agents or other valvle surgery procedures with global good clinical results.
From the first case of primitive cardiac surgery (CS), treatment of stab wound of the heart (Dr. Daniel Hale Williams, 1893), to recent surgical procedures and device implantations for end-stage heart failure (HF), the CS has grown and emerged in the public health more and more [1].
The heart valve disease had interested immediately since the non-cardiopulmonary era because of the multitude of rheumatic patients and congenital valve disease. In the 1952, Hufnagel implanted the first valve in descending aorta and it was the sign of the first step of the CS evolution. New prosthesis and heart valve techniques were tested between 1970 and 2000 with optimal results in patients’ quality of life and survival, at the same time of CPB evolution.
Whilst, the evolution of heart valve surgery had stimulated new devices, prosthesis and the development of minimally invasive surgery, this was partially diminished by the spreading of trans catheter valve implantation. In the 2002, Dr. Alain Crabbier described a non-surgical prosthetic valve implantation firstly: it was the revolution of CS evolution [2]. The transcatheter valve implantation has evolved and spread rapidly with multiple approaches femoral to apical, aortic, axillary and carotid, and many suitable and technological devices. The higher and higher risk patients, the needs to avoid surgical complications, the evolution of available devices and the fabrication of new technologies have increased the efforts to improve trans catheter valve implantation [3].
The recent article of Loyalka et al, described a special case of tricuspid valve in valve replacement with Sapien 3, an innovative and alternative therapeutic choice to a tricuspid valve degeneration [4]. Instead, Sawara et al [5], documented as trans catheter aortic valve implantation for a failing surgical bio prosthesis or native aortic valve regurgitation has become an alternative for patients at high risk for redo surgical aortic valve replacement or aortic regurgitation since now off-label: that was a reliable and significant results in the era of trans catheter valve implantations.
What would we attend from the future? In the most surgical centres, the trend were a significant decrease in patients undergoing to open-heart valve surgery compared to trans catheter valve implantation.
Maybe the new ongoing studies of lower and mild-risk patients undergone to transcatheter procedure would open either a deeper collaboration of the heart team and a new therapeutic perspectives in the public health with a shift to more minimally invasive procedures, less day of hospitalization and I don’t see why not less costs for public health.
Background: Herbal essential oil contains pharmacological benefits for intervention treatment of various diseases. Studies have demonstrated its antimicrobial, antioxidant, and anti-inflammatory effect involving in vitro cell culture and preclinical animal models. It has been also traditionally used to reduce anxiety and hypertension in human. However, scientific studies elucidating its mechanism of action and pharmacological targets, as well as its effectiveness and safety as phytotherapeutic compounds are still progressing. Recent studies showed its promising effect in depression-cardiovascular disease intervention. However, comprehensive evaluations to enlighten latest advancement and potential of herbal essential oil are still lacking.
Objective: In this systematic review, the depression-cardiovascular effects of herbal essential oil on lipid profile, biochemical and physiological parameters (e.g haemodynamic) are presented. The route of delivery and mechanism of action as well as main bioactive compounds present in respective essential oil are discussed.
Methods: Article searches are made using NCBI PubMed, PubMed Health, SCOPUS, Wiley Online, tandfonline, ScienceDirect and Espacenet for relevant studies and intellectual properties related to essential oil, depression and cardiovascular disease.
Results: In experimentation involving in vitro, in vivo and clinical trials, herbal essential oil showed its effectiveness in reducing coronary artery disease (narrowing of the arteries), heart attack, abnormal heart rhythms, or arrhythmias, heart failure, heart valve disease, congenital heart disease, heart muscle disease (cardiomyopathy), pericardial disease, aorta disease, Marfan syndrome and vascular (blood vessel) disease.
Conclusion: This review gives a valuable insight on the potential of essential oil in the intervention of depression associated with cardiovascular diseases. Studies showed that herbal essential oil could act as vasodepressor, calcium channel blocker, antihyperlipidemia, anticoagulant, antiatherogenesis and antithrombotic. It can be proposed as an interventional therapy for depression-cardiovascular disease to reduce doses and long-term side-effect of current pharmacological approach.
The normal levels of thyroid hormones (THs; thyroxine, T4 & 3,5,3′-triiodo-L-thyronine, T3) are necessary for the normal development [1-48], particularly the fetal and neonatal cardiac growth and development [49]. The actions of THs are facilitated genomically by thyroid receptors (TRs, α and β) and non-genomically at the plasma membrane, in the cytoplasm and in cellular organelles [4,49-55], by stimulation of Na+, K+, Ca2+ and glucose transport, activation of protein kinase C (PKC), protein kinase A (PKA) and mitogen activated and protein kinase (ERK/MAPK) [4]. In addition, the transport of T4 and T3 in and out of cells is controlled by several classes of transmembrane TH-transporters (THTs) [56], including members of the organic anion transporter family (OATP), L-type amino acid transporters (LATs), Na+/Taurocholate cotransporting polypeptide (NTCP), and monocarboxylate transporters (MCTs) [4,49,57,58]. Adding additional complexity, the metabolism of T4 and T3 is regulated by 3 selenoenzyme iodothyronine deiodinases (Ds: D1, D2 and D3) [59-61]. On the other hand, the congenital hypothyroidism can cause the following [49,62-64], (1) congenital heart diseases; (2) diastolic hypertension; (3) reduced cardiac output, stroke volume and a narrow pulse pressure; (4) dilatation and overt heart failure; (5) elevation in the systemic vascular resistance [65-68]. Similarly, the chronic hyperthyroidism can cause the following [49,64]: (1) cardiac hypertrophy; (2) increase in the cardiomyocyte (CM) length rather than width; (3) noticeable diminution in systemic vascular resistance; (4) elevation in the cardiac contractility; (5) systolic hypertension; (6) increase in the cardiac output, venous volume return, blood volume and pulse pressure; and (7) reduction in the systemic vascular resistance [49,69]. T3-therapy can induce DNA synthesis and cardiomyocyte proliferation, and improve the cardiac contractility; though, this action is as still unidentified [49,70-74].
The infectivity and pathogenesis: SARS-CoV-2, the causative agent of Covid-19, involves Angiotensin-converting enzyme 2 (ACE2) receptors on type II alveolar type 2 (AT2) cells in lungs. Apart from, the upper and lower respiratory tracts, the disease affects the gastrointestinal system prominently, as evidenced by the significant GI symptoms, early in the course of the disease. In addition, the virus infects ACE2-bearing cells in other organs including the heart and blood vessels, brain, and kidneys.
Clinical features and morbidity: The clinical spectrum of COVID-19 varies from asymptomatic or pauci-symptomatic presentation to moderate to severe states characterized by respiratory failure necessitating mechanical ventilation and ICU support and those manifesting critical clinical condition with complications like sepsis, septic shock, and multiple organ dysfunction failure. The CT chest is an important tool for early identification of COVID-19 pneumonia as well as for prognostic purposes.
The recovery and residual damage: The recovery and other outcomes vary depending on age and other aspects including sex, comorbidities, and genetic factors. The outlook for older adults, who account for a disproportionate share of critical disease, is unfavorable, and most of those who survive are unlikely to return to their previous level of functioning. The disease affects their long-term health and quality of life as well as brings in propensity for truncated post-disease survival.
COVID-19 aftermath and follow up: The patients discharged from hospital following severe COVID-19, continue to suffer with lingering impact of the disease as well as that of the emergency treatments that saved their life. The post-infection reduced exercise tolerance and other subtle factors, like post viral fatigue syndrome, post-traumatic stress disorder, impaired concentration, delirium, and disturbed sleep-wake cycle often underly the functional impairment. In fact, there is need of step-down care and later a multidisciplinary support involving regular clinical assessment, respiratory review, physiotherapy, nutritional advice, and psychiatric support.
Conclusion: The life after COVID-19: After recovery from the disease, the virus SARS-CoV-2, may persist for uncertain period. In addition, the chance of reinfection cannot be ruled out. The vitamin D supplementation may be helpful. In general, the quality of life (QOL) in ICU survivors improves but remains lower than general population levels, but most of the patients adapt well to their level of self-sufficiency and QOL. Also, the debility due to co-morbidities may further compromise the activity of daily living and QOL issues. The Age and severity of illness appear to be the major predictors of post-discharge physical functioning.
As per report of WHO [1] (World Health Organization), air pollution (ambient/outdoor and household/indoor air pollution) kills an estimated seven million people worldwide every year largely as a result of increased mortality from stroke, heart disease, chronic obstructive pulmonary disease, lung cancer and acute respiratory infections. Data of WHO shows that 9 out of 10 people breathe air containing high levels of pollutants. World Health Organization is working with countries to monitor air pollution and improve air quality. From smog hanging over cities to smoke inside the home, air pollution poses a major threat to health and climate. More than 80% of people living in urban areas and around 91% of the world’s population live in places where air quality levels exceed WHO limits, with developing and under-developed countries suffering from the highest exposures, both indoors and outdoors [1]. While outdoor air pollution comes from the motor vehicles, burning of fossil fuels and other industrialization activities, indoor air pollution is the result of tobacco smoke and burning fuel for cooking & heating. Furniture and construction materials also emit such pollutants. Both outdoor and indoor air pollution are harmful to the human health.
Hypertension is a complex disorder involving multiple organ systems and the primarily modifiable risk factor for heart disease, which is the leading cause of death among both men and women in the World. Although both men and women develop hypertension, distinct gender differences in the incidence and severity of hypertension are well established where men have a higher incidence of hypertension compared with women of the same age until the sixth decade of life [1,2]. Despite gender differences in human hypertension, the treatment guidelines do not differ by gender [3]. Even if the causes of hypertension are complex and are related to genetic factors, lifestyle, diet structure, and environmental factors including air pollution [4], coupled with the potential determinants of hypertension, sex differences in hypertension-which exist in human populations-are attributed to both biological and behavioural factors. The biological factors include sex hormones, chromosomal differences, and other biological sex differences that are protective against hypertension in women. These factors become prominent in adolescence and persist through adulthood until women reach menopause. Behavioural risk factors for hypertension include high body mass index, smoking, and low physical activity.
Hypertension and blood pressure are closely related, and hypertension is directly related with stroke. There are different type of blood pressures such as basal, diastolic, maximum, mean arterial, systolic, mean central venous. The present report examines the determinants of systolic blood pressure for two different groups of cardiac patients. One group of cardiac patients is those who underwent dobutamine stress echocardiography, and the other group is Worcester heart attack study. Many systolic blood pressure determinants, their effects, and correlations have been focused in the current report.
In this review After Observing biomedical literature (starting from some heart disease) results that some pathological phenomena are deeply involved in some metabolic endocrine condition: Kinetics and gradients in metabolism, catabolism, time related, toxic like effect, electrical cell membrane status, smooth vascular muscle cell hyper-reactivity, platelet iperactivations, central autonomic control after acute stroke, great electrolytes unbalances et other factors as pro-hypertrophic signaling and oxidative stress. Observing actual current therapy in some metabolic endocrine therapy often is used association of drugs (in example in type II diabetes). In Many other pathologies efficacy drug therapy exist, and often only 1 pharmacological molecule resolve the pathological condition. But in many disease even associating 2-3-4 drugs the % of cure not increase (efficacy, effectiveness). It mean that this drugs strategies are not the really best? Or it mean a low active level? Why for this pathological condition this association drugs in currently use not do the right works as really needed? There is the need for new really efficacy drugs strategy that show a profile of efficacy as requested in order to resolve the pathological condition? Or to be added to the actual therapy? The actual pharmacological strategies in some metabolic endocrine disorder is really the best? Or other strategies can be introduced?
Previous clinical, observation and epidemiologic studies have demonstrated strong association between serum uric acid (SUA) and cardiovascular disease (hypertension, heart failure, and asymptomatic atherosclerosis), metabolic states (abdominal obesity, diabetes mellitus, metabolic syndrome, insulin resistance) and kidney disease. There is a large body of evidence regarding the role of SUA as predictor of CV events and CV mortality in general population and individuals with established CV disease and metabolic diseases. However, SUA may exhibit protective effects on endothelium and vasculature as well as attenuate endogenous repair system through mobbing and differentiation of cell precursors. Although SUA lowering drugs are widely used in patients with symptomatic hyperuricemia and gout beyond their etiologies, there is no agreement of SUA below target level 6.0 mg/dL in asymptomatic individuals with kidney injury and CV disease and data of ones are sufficiently limited. The short communication is depicted on the controversial role of SUA as primary cell toxicity agent and secondary cell protector against hypoxia, ischemia and apoptosis
Gabriela Borrayo-Sánchez*, Martin Rosas-Peralta, Janaí Santiago-López, Erick Ramirez Árias, Rosalba García Méndez, Victor Hugo Borja-Aburto, Ana Carolina Sepúlveda-Vildósola and José de Jesús Arriaga-Dávila
The new report of American College of Cardiology/American Heart Association task force on Clinical Practice Guidelines for High Blood Pressure in Adults was published online ahead of print November 13, 2017. The new American recommendation was focused on the criteria to define Hypertension. 130/80 mmHg or more is now considered as the new cut off point to define Hypertension. It is not new if we consider cumulative evidence in the las two decades has been broken the idea to consider 140/90 mmHg as the point to start medical actions. Thus, in México with current ACC/AHA definition it is estimated today around 48 million of adult hypertensive population. In the Mexican Institute of Social Security (IMSS) several strategies has been developed to improve prevention as the key action to confront non communicable chronic disease including hypertension. This updated guideline from ACC/AHA is an extraordinary opportunity to reinforce our preventive programs to high blood pressure control. In this brief report we analyze the epidemiological situation in Mexico and its possible consequences of the new criteria for hypertension diagnosis. The main current strategies that are applied into the IMSS to confront cardiovascular risk factors are directed to prevention. The IMSS is prepared to attend situations as the change of criteria diagnoses in Hypertension and new preventive models are in progression.
Gabriela Borrayo-Sánchez*, Martin Rosas-Peralta, Erick Ramírez-Arias, Gladys M Jiménez-Genchi, Martha Alicia Hernández-Gonzále, Rafael Barraza-Félix, Lidia Evangelina Betacourt-Hernández, ocio Camacho-Casillas, Rodolfo Parra-Michel, Héctor David Martínez Chapa and José de Jesús Arriaga-Dávila
Atherosclerotic cardiovascular disease (ASCVD) is globally defined as coronary heart disease, cerebrovascular disease, or peripheral arterial disease presumed to be of atherosclerotic origin and it is the leading cause of morbidity and mortality for individuals with or without diabetes and is the largest contributor to the direct and indirect catastrophic costs of cardiovascular disorder. Very common conditions coexisting into the cardiovascular risk (e.g., obesity, hypertension, diabetes and dyslipidemia) are clear risk factors for ASCVD, and diabetes itself confers independent risk. Numerous studies have shown the efficacy of controlling individual cardiovascular risk factors in preventing or slowing ASCVD in people with these disorders. In other words it is not enough control one risk factor. We need to develop novel strategies to detect and control all of them at the same time. Thus, large benefits are seen when multiple cardiovascular risk factors are addressed simultaneously. Under the current paradigm of aggressive risk factor modification in patients with cardiovascular risk, there is evidence that measures of 10-year coronary heart disease (CHD) risk among U.S. adults with cardiovascular risk have improved significantly over the past decade and that ASCVD morbidity and mortality have decreased. In Mexico the Mexican Institute of Social Security is implementing new strategies of primary and secondary prevention in order to confront this pandemic.
In this review, we analyze the state of the art to approach at the same time the different cardiovascular risk factors, in an integral form because of this is the real worldwide challenge of health.
Hypertension is one of the most common chronic diseases of human, affecting more than one billion people worldwide. When it becomes chronic, hypertension leaves behind cardiac hypertrophy, heart failure, stroke, and kidney disease, resulting in substantial morbidity and mortality. Treatments that effectively reduce blood pressure can prevent these complications. Abnormalities in the production of urine by the kidneys have been implicated in increased vascular resistance, leading to high blood pressure and increased cardiac mass. By matching urinary excretion of salt and water with dietary intake, balance is usually attained, thereby maintaining a constant extracellular fluid volume and blood pressure. Based on the capacity for the kidney to excrete sodium, this blood pressure-altering mechanism should have sufficient advantage to limit intravascular volume and consequently lower blood pressure in response to a range of stimuli from elevated heart rate to increase peripheral vascular resistance. A major determinant of the level of intra- and extra- renal blood pressure is therefore sodium handling, and it is controlled by complex physiological mechanism by hormones, inflammatory mediators, and the sympathetic nervous system. Homoeostasis and favourable influence sodium balance are a basic mechanism of efficacy for diuretics and dietary sodium restriction in hypertension. Renin Angiotensin System (RAS) inhibitors, vasodilators, and β-blockers work to facilitate pressure-natriuresis. Also, WNK signaling pathways, soluble inflammatory mediators, and pathways regulating extra-renal sodium disposition may be the focus towards elimination of sodium and reducing blood pressure in hypertension.
Background: Several epidemiologic studies indicate that up to 50% of patients with heart failure have a preserved ejection fraction, and this proportion has increased over time. The knowledge of its severity and associated comorbidity is determining factor to develop adequate strategies for its treatment and prevention. This study was focus on the creation of a cohort and follow-up of Mexican population and to analyze its severity as well as its interaction with the comorbidity of other cardiovascular risk factors.
Methods: We included patients from different sites of Mexico City than were sent to the Cardiology hospital of the National Medical Center in Mexico City for the realization of an echocardiogram as part of their assessment by the presence of dyspnea, edema, or suspicion of hypertensive heart disease. Complete medical history, physical examination and laboratory studies including Brain Natriuretic Peptide (BNP) serum levels were performed. Diagnosis of diastolic dysfunction was based on symptoms and echocardiographic data including time of deceleration, size of left atrium, e´ septal and e´ lateral, as well as E wave, A wave and its ratio E/A. All patients had left ventricle ejection fraction > 45%.
Results: We included 168 patients with HFpEF. The most common risk factor was hypertension (89.2%), followed by overweight and obesity (> 78.5%), dyslipidemia (82.1%) and diabetes (42.8%). Women were dominant, 108 (64.3%); the mean age was 63 years old. When we classify by severity of diastolic dysfunction, we found that 41.1% were grade I, 57.1% were grade II and only 1.8% were grade III. The risk factors most strongly associated with the severity of diastolic dysfunction were hypertension, obesity and dyslipidemia. We found BNP levels highly variables, but the levels were higher detected as the ejection fraction was approaching to 45%. At one year of follow up mortality was not reported.
Conclusion: HFpEF is a frequent entity in patients with cardiovascular risk factors in Mexico. The most common risk factor was hypertension. The combination of hypertension, overweight and dyslipidemia predicted the severity of diastolic dysfunction. We recommend that all Mexican patient with hypertension and overweight or obesity should be submitted as a part of its medical evaluation to an echocardiogram study in order to detect diastolic dysfunction even though the signs or symptoms are or not evident.
Martin Rosas-Peralta*, Luis Alcocer, Humberto Álvarez-López, Gabriela Borrayo-Sánchez, Ernesto Germán Cardona-Muñoz, Adolfo Chávez-Mendoza, Enrique Díaz y Díaz, José Manuel Enciso-Muñoz, Héctor Galván-Oseguera, Enrique Gómez-Álvarez, Pedro Gutiérrez-Fajardo, Héctor Hernández y Hernández, Francisco Javier León-Hernández, José Antonio Magaña-Serrano and José Zacarías Parra-Carrillo
Today, Mexico has more than 130 million inhabitants; 85 millions of them are adults of 20 or more years old. The population pyramid is still one of base wider and this base corresponds to adults younger than 54 years old. Despite predictions made 20 years ago, about a transformation of the population pyramid shape to a mushroom shape as a consequence of more life expected and adult population growth; this change has not been occurred. Hypertension has become the biggest challenge of noncommunicable chronic diseases to public health in Mexico. Around 30% of adult Mexican population has hypertension; 75% of them have less than 54 years old (in productive age); 40% of them are unaware but only 50% of aware hypertensive population takes drugs and, 50% of them are controlled (< 140/90 mmHg). Cardiovascular risk factors including hypertension, dyslipidemia, obesity, and diabetes often cohabit in the same person and are magnified one to another in terms of common pathophysiological pathways. Atherosclerosis, arrhythmias, stroke and heart failure are common and are the final pathologic end-points and explains why cardiovascular diseases occupy first place in mortality in Mexico and worldwide. The costs of care for these diseases are billionaires and if we do not generate appropriate strategies, their global impact can become a high threat to social development of the country. The life style like nutrition, sports habits of the Mexicans must be emphasized; there is poor education about this crucial topic. This position paper is focused on the principal controversies and strategies to be developed by all, government, society, physicians, nurses, patients and all people related with healthcare of hypertension, in order to confront this huge public health problem in Mexico.
The European Society of Cardiology (ESC) and the European Society of Hypertension (ESH) jointly developed a series of hypertension guidelines in the years 2003, 207 and 2013. The most recent guidelines were issued by the two societies in August this year (2018) and were published in the European Heart Journal. The new guidelines are printed in more than 90 pages and cover almost all aspects of hypertension based on extensive review of literature giving highest priority to data from randomized controlled trials and well conducted meta-analysis. In important areas where there is inadequate or no evidence, guidelines authors resort to expert opinion. The text was developed over approximately 24 months and was reviewed by representatives of ESC and ESH national hypertension societies. Although it is less than five years since the last hypertension European guidelines in 2013, the recent 2018 guidelines show important differences in diagnosis and treatment strategies with the addition of new sections and recommendations on management of hypertensive emergencies, hypertension in women and pregnancy, different ethnic groups, chronic obstructive pulmonary disease, cancer therapies, peri-operative management, sexual dysfunction and perioperative management.
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