The Association of Desert Dust with the Risk of Acute Coronary Syndrome in Subjects of a Younger Age.

Objectives: Recently, desert dust in Europe has been recognized as a cardiovascular health problem. In Spain, desert dust inflows in recent years have been associated with worsening air quality. The present study examines whether desert dust events are related to the incidence of acute coronary syndrome (ACS) in patients under 55 years of age. Methods: Data from 2416 consecutive patients admitted to a tertiary hospital due to ACS were prospectively analyzed. A case-crossover time-stratified design using Poisson conditional regression models was applied to estimate the impact of desert dust events involving particulate matter concentrations of an aerodynamic diameter <10 µm (PM10) on the incidence of ACS in patients under 55 years of age. Results: Desert dust intrusion on days 0 to 5 before ACS onset showed no significant association with the incidence of ACS in patients under 55 years of age. The incidence rate ratios of PM10 concentrations 1, 2, 3, 3, 4, and 5 days before ACS onset (for changes of 10 µg/m3) were 1.02 (95% CI 0.97-1.1; p = 0.41), 1.01 (95% CI 0.96-1.07; p = 0.66), 0.99 (95% CI 0.94-1.05; p = 0.78), 0.96 (95% CI 0.9-1.02; p = 0.18), and 0.97 (95% CI 0.91-1.04; p = 0.41). Conclusions: Our findings suggest that desert dust is unlikely to be related to the incidence of ACS in patients under 55 years of age.

Late bleeding events in TAVI patients receiving vitamin K antagonists or direct oral anticoagulants.

INTRODUCTION AND OBJECTIVES: The optimal chronic antithrombotic regimen for patients with atrial fibrillation undergoing transcatheter aortic valve implantation (TAVI) remains uncertain. Our aim was to compare the incidence of late bleeding events between patients on direct oral anticoagulants (DOACs) and those on vitamin-K antagonists (VKA). METHODS: This single-center observational study included TAVI patients requiring oral anticoagulation at discharge between 2015 and 2021. The primary endpoint was any clinically significant bleeding event. Secondary endpoints were stroke, heart failure, and all-cause mortality. RESULTS: A total of 702 TAVI procedures were performed, with 297 patients requiring oral anticoagulation at discharge. Among them, 206 (69.4%) received VKA and 91 (30.6%) received DOAC. Baseline clinical, procedural and in-hospital characteristics did not significantly differ between groups, except for better renal function among DOAC patients. The median length of follow-up was 2.8 years. The risk of bleeding events was higher in patients receiving DOACs than in those receiving VKA (HR, 2.27; 95%CI, 1.21-4.26; incidence of 9.7 and 4.2 events per 100 patient-years of follow-up for DOAC and VKA patients, respectively). There were no statistically significant differences in the rates of stroke (HR, 1.28; 95%CI, 0.4-4.3), heart failure hospitalization (HR, 0.92; 95%CI, 0.46-1.86), or all-cause mortality (HR, 1.02; 95%CI, 0.68-1.55). CONCLUSIONS: In older patients undergoing TAVI and receiving anticoagulant therapy for atrial fibrillation, the use of DOAC was associated with a higher risk of late bleeding events than VKA.

Hemodynamic performance of self-expandable transcatheter aortic valve replacement systems during valve deployment.

OBJECTIVES: Little is known about valve hemodynamic performance during the Evolut and Neo deployment course. We aimed to evaluate transvalvular mean and peak-to-peak gradients over several intraprocedural timepoints during TAVR with Evolut PRO+ (Medtronic) and Neo (Boston Scientific) systems. METHODS: This was single-center pilot sub-study from the SavvyWire EFficacy and SafEty in Transcatheter Aortic Valve Implantation Procedures (SAFE-TAVI) trial. Participants received either the Evolut PRO+ or Neo for native valve severe aortic stenosis and the SavvyWire (OpSens Medical) was used for device delivery, pacing, and continuous left ventricular and aortic pressure measurements. For the Evolut, evaluation was done for baseline, two-thirds of valve deployment (still recapturable), 90% of valve deployment (no longer recapturable), and post-deployment hemodynamics. For the Neo, analysis was done at baseline, after the first step (top-crown deployment), and at final status. RESULTS: Nineteen patients were included (Evolut = 15; Neo = 4). There were no statistically significant changes in peak-to-peak gradients (44 mm Hg [IQR:33-69] vs 43 mm Hg [IQR:26-62], P = .41) between baseline and two-thirds of valve deployment in the Evolut patients. There was a significant decrease in mean (40 mm Hg [IQR:32-54] vs 14 mm Hg [IQR:10-18], P less than .001) and peak-to-peak (43 mmHg [IQRS:26-62] vs 9 mm Hg [IQR:8-13], P less than .001) transvalvular gradients between two-thirds and 90% of valve deployment for Evolut. Neo patients exhibited a decrease in transvalvular gradients after top-crown deployment (42.5 mm Hg baseline vs 13 mm Hg). CONCLUSIONS: Transvalvular gradients did not vary between the point of "no-recapture" compared to baseline values in patients receiving the Evolut, whereas a significant reduction in transvalvular gradients was observed when the valve was deployed at 90% and fully deployed. The Neo valve was slightly obstructive after the first step of deployment.

Natural History of Dilated Cardiomyopathy Due to c.77T>C (p.Val26Ala) in Emerin Protein.

(1) Introduction: Dilated cardiomyopathy (DCM) mainly affects young individuals and is the main indication of heart transplantation. The variant c.77T>C (p.Val26Ala) of the gene coding for emerin (EMD) in chromosome Xq28 has been catalogued as a pathogenic variant for the development of DCM, exhibiting an X-linked inheritance pattern. (2) Methods: A retrospective study was conducted covering the period 2015-2023 in patients with DCM of genetic origin. The primary endpoint was patient age at onset of the first composite major cardiac event, in the form of a first episode of heart failure, malignant ventricular arrhythmia, or end-stage heart failure, according to the presence of truncating variant in titin gene (TTNtv) versus the p.Val26Ala mutation in the EMD protein. (3) Results: A total of 31 and 22 patients were included in the EMD group and TTNtv group, respectively. The primary endpoint was significantly higher in the EMD group, with a hazard ratio of 4.16 (95% confidence interval: 1.83-9.46; p = 0.001). At 55 years of age, all the patients in the EMD group had already presented heart failure, nine presented malignant ventricular arrhythmia (29%), and 13 required heart transplantation (42%). (4) Conclusions: DCM secondary to the c.77T>C (p.Val26Ala) mutation in the EMD gene is associated to an increased risk of major cardiac events compared to patients with DCM due to TTNtv, with a large proportion of transplanted patients in the fifth decade of life.

"Inherited cardiovascular disease mindset" can identify concealed inherited conditions at cardio-oncology evaluation: An opportunistic screening.

INTRODUCTION: Baseline cardiovascular (CV) risk stratification is recommended in all cancer patients. Integrating all clinical information (personal/family history, ECG and echocardiogram) can properly identify high-risk patients. We aimed to evaluate the concealed inherited CV conditions detected in mandatory CV screening performed at a Cardio-Oncology Unit. METHODS: retrospective study of all consecutive cancer patients referred to the Cardio-Oncology Unit for CV evaluation (2020-2023). Inherited CV conditions diagnosis and genetic testing was performed according to guidelines. RESULTS: 1984 cancer patients underwent CV screening. Sanger sequencing was indicated in 1 patient, excluding the genetic family disease. NGS sequencing was performed in 11 cancer patients with normal left ventricular ejection fraction (LVEF): 2 due to aortic syndrome evaluation (identifying 1 vascular Ehrler-Danlos syndrome due to COL3A1 p.Arg242Ter), 4 channelopathies (2 Long QT syndrome and 2 Brugada's), 4 hypertrophic cardiomyopathies and 1 non-dilated left ventricular cardiomyopathy (NDLVC). Among the 12 patients with reduced LVEF, one was diagnosed with NDLVC, and chemotherapy-induced dilated cardiomyopathy was only ascribable in 3 of them. CONCLUSION: Integrating clinical information at mandatory baseline CV toxicity risk cardio-oncology evaluation, can identify high-risk cancer patients with concealed inherited conditions. Keeping an "inherited cardiovascular disease-oriented mindset" to implement opportunist screenings is encouraged.

Optimal oversizing in transcatheter aortic valve replacement with the self-expanding Evolut valve system.

OBJECTIVES: Valve oversizing has been associated with reduced paravalvular leaks (PVL) and valve migration risk. However, no optimal cut-off oversizing value has been defined for the Evolut system (Medtronic). The aim of this study was to assess the relationship between the degree of oversizing and moderate-to-severe PVL and determine the optimal oversizing cut-off value. METHODS: We conducted a multicenter study that included 740 consecutive patients with multidetector computed tomography (CT) data. Valve size was selected according to manufacturer recommendations, with oversizing ranging from 10% to 30%. The primary endpoint was moderate-to-severe PVL. RESULTS: The median age was 84 years (79-87 years), with 58.4% women, and a median EuroSCORE II of 4.1% (2.4-7.3%). Moderate-to-severe PVL was observed in 7.0% of the patients. An inverse relationship was found between oversizing and both PVL (11.3%, 8.6%, 5.4%, and 2.7% for quartiles Q1 to Q4; P = .007) and the need for post-dilation (P = .016). The multivariable analysis showed an association between oversizing and PVL (OR: 0.915 for each 1%-increase, P = .002). The optimal oversizing cut-off value to predict PVL was 20%, and PVL was significantly higher in patients with oversizing less than 20% (10.5% vs.4.2%, P less than .001). There were no differences in major clinical events according to the degree of oversizing, and a higher oversizing did not translate into an increased risk of permanent pacemaker (18.4% vs18.3%, P = .976). CONCLUSIONS: In TAVR with the Evolut valve, a higher oversizing was associated with lower rates of moderate-to-severe PVL and a lower need for post-dilation, with no negative impact on procedural and early clinical outcomes. A 20% oversizing threshold could be suggested to reduce PVLs. Further prospective studies are warranted to validate optimal oversizing for this valve system.

Survival analysis and gender differences in hypertrophic cardiomyopathy proband patients referred for genetic testing.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is believed to have low overall mortality rate, that could be influenced by gender, particularly among probands. We aimed to evaluate the survival rates and possible gender differences in a homogeneous cohort of HCM proband patients, referred for genetic testing, from the same geographical area, without differences in medical care access nor clinical referral pathways. METHODS: we compared the mortality rates of a cohort of consecutive HCM probands referred for genetic testing (2000-2022), from a Spanish region (xxx1) with a centralized genetic testing pathway, with its control reference population by Ederer II method. Gender differences were analyzed. RESULTS: Among the 649 HCM probands included in this study, there were significantly more men than women (61.3% vs 38.7, p < 0.05), with an earlier diagnosis (53.5 vs 61.1 years old, p < 0.05). Clinical evolution or arrhythmogenic HCM profile did no show no significant gender differences. Mean follow up was 9,8 years ±6,6 SD (9,9 ± 7 vs 9,6 ± 6,1, p = 0.59). No statistically significant differences in observed mortality, expected survival and excess mortality were found in the general HCM proband cohort. However, we found a significant excess mortality in female probands with HCM. No additional differences in analysis by genetic status were identified. CONCLUSION: Expected survival in our HCM probands did not differ from its reference population. However, despite no gender differences in phenotype severity were identified, proband HCM women did present a diagnosis delay and worse mortality outcomes.

PCSK9 gene variations in the clinical setting of premature cardiovascular disease: A critical appraisal.

INTRODUCTION: Information about PCSK9 gene variations and its association with cardiovascular (CV) disease is controversial. We aimed to evaluate 3 reported polymorphisms in PSCK9 in a cohort of young patients with myocardial infarction with ST segment elevation (STEMI). METHODS: Retrospective study of consecutive patients with premature STEMI (2018-2023). 216 patients with STEMI due atherothrombotic coronary artery disease (CAD), confirmed by coronary angiogram, were included. We genotyped 3 polymorphisms in PCSK9 (rs12117661, rs2483205, rs505151) in 207 patients (DNA unavailable in 9) and a control group (N = 200). RESULTS: Mean age 49.4 ± 6,6 years (82.4% men). Genotypes frequencies distribution in patient's and control's cohorts did not deviate from the expected by Hardy-Weinberg equilibrium and there were no significant differences between patients and controls. Among patients, we did not find any association between PSCK9 genotypes and clinical variables (gender, age, CV risk factors, cholesterol levels, family history of premature CAD or number of coronary arteries affected). CONCLUSION: We did not find any association between PSCK9 genotypes (RS12117661, RS2483205 and RS505151) and any CV risk factors or the extent of CAD in a cohort of patients with premature STEMI. There were not differences in the genotype distribution between patients and controls.

Sex-Related Differences in Life Expectancy Compared to General Population after Surgery for Ascending Aortic Aneurysm.

Background/Objectives: Understanding sex-based differences in cardiovascular outcomes is paramount to improving clinical outcomes. Surgery is an aggressive but effective therapy for ascending aortic aneurysm. We sought to determine if being a woman is a risk factor for long-term mortality after this surgery. We compared their life expectancy with a general population of the same age, sex, year, and region. Methods: We compared men and women undergoing AAA surgery at our institution from 2000 to 2019. After balancing the population with propensity score (PS) matching, we compared long-term mortality control with a Cox regression. We determined the RS using the Ederer II method and compared it to a healthy reference population of the same age, sex, and region. Results: From 2000 to 2019, 232 women and 506 men underwent ascending aortic aneurysm surgery. After a mean follow-up of 51.5 ± 34.5 months, sex was not an independent risk factor for long-term mortality in the multivariable analysis [HR: 0.68 (95% CI 0.43-1.07, p = 0.23)]. Matching by baseline characteristics, 196 pairs were analyzed with no differences regarding mortality in the Cox regression [HR: 1.11 (95% CI 0.65-1.9, p = 0.23)]. Men and women who survived the postoperative period presented a relative survival of 100.3% (95% CI 97.4-101%) and 100.3% (95% CI 98.9-101.1%), respectively, similar to the reference population without the disease. Conclusions: For patients undergoing AAA surgery, sex was not an independent predictor of mortality. Men and women who survived the postoperative period presented a similar life expectancy to that of the reference population (people free from the disease of the same age, sex, year, and region).

Combined Use of MITRACLIP and Ventricular ASSIST Devices in Cardiogenic Shock: MITRA-ASSIST Registry.

Background: Patients with cardiogenic shock (CS) and mitral regurgitation (MI) have a prohibitive risk that contraindicates surgical treatment. Although the feasibility of transcatheter edge-to-edge therapy (TEER) has been demonstrated in this setting, the benefit of the combined use of TEER with mechanical circulatory support devices (MCS) has not been studied. The aim of this study was to evaluate the clinical outcomes of TEER in patients with MCS. Methods: The MITRA-ASSIST study is a retrospective multicentre Spanish registry that included patients with MR and CS who underwent TEER in combination with MCS. The primary endpoint was death from any cause at 12 months. The secondary endpoint was a composite of death from any cause or hospitalisation for heart failure at 12 months. Results: A total of twenty-four patients in nine high-volume Spanish centres (66.2 (51-82) years, 70.8% female, EuroSCORE II 20.4 ± 17.8) were included. Acute ST-elevation myocardial infarction was the main CS aetiology (56%), and the most implanted MCS was the intra-aortic balloon pump (82.6%), followed by ECMO (8.7%), IMPELLACP® (4.3%), or a combination of both (4.3%). Procedural success was 95.8%, with 87.5% in-hospital survival. At 12-month follow-up, 25.0% of patients died, and 33.3% had a composite event of death from any cause or hospitalisation for heart failure. Conclusions: TEER in patients with concomitant CS and MR who require MCS appears to be a promising therapeutic alternative with a high device procedural success rate and acceptable mortality and heart failure readmission rates at follow-up.

Concealed Inherited Cardiomyopathies Detected in Cardio-Oncology Screening.

INTRODUCTION: Basal cardiovascular risk assessment in cardio-oncology is essential. Integrating clinical information, ECG and transthoracic echocardiogram can identify concealed inherited cardiomyopathies (ICMPs) with potential added risk of cardiotoxicity. We aimed to evaluate the impact of our Cardio-Oncology Unit design in detecting concealed ICMPs. METHODS: We carried out a retrospective study of all consecutive breast cancer patients referred to the Cardio-Oncology Unit for cardiac evaluation (2020-2022). ICMPs diagnosis was provided according to ESC guidelines and underwent genetic testing. ICMPs prevalence in this cohort was compared to the highest and lowest frequency reported in the general population. RESULTS: Among 591 breast cancer patients, we identified eight patients with ICMPs: one arrhythmogenic cardiomyopathy (ACM), three familial non-ischemic dilated cardiomyopathy (DCM), three hypertrophic cardiomyopathy (HCM) and one left ventricular non-compaction cardiomyopathy (LVNC), which has now been reclassified as non-dilated left ventricular cardiomyopathy. The number of ICMPs identified was within the expected range (neither overdiagnosed nor overlooked): ACM 0.0017 vs. 0.0002-0.001 (p 0.01-0.593); DCM 0.0051 vs. 0.002-0.0051 (p 0.094-0.676); HCM 0.005 vs. 0.0002-0.002 (p < 0.001-0.099); LVCN 0.0017 vs. 0.00014-0.013 (p 0.011-0.015). Genetic testing identified a pathogenic FLNC variant and two pathogenic TTN variants. CONCLUSION: Opportunistic screening of ICMPs during basal cardiovascular risk assessment can identify high-risk cancer patients who benefit from personalized medicine and enables extension of prevention strategies to all available relatives at concealed high cardiovascular risk.

Impacto del polvo sahariano en la incidencia de síndrome coronario agudo / Impact of Saharan dust on the incidence of acute coronary syndrome

Introducción y objetivos Recientemente, el polvo desértico se ha reconocido en Asia como desencadenante de infarto agudo de miocardio. En España, las entradas de polvo sahariano están relacionadas con empeoramientos de la calidad del aire debidos a aumentos en las concentraciones de material particulado en el aire ambiental. Nuestro objetivo es dilucidar si los eventos de polvo sahariano tienen relación con la incidencia de síndrome coronario agudo (SCA) en pacientes que habitan cerca del norte de África, la mayor fuente global de polvo desértico. Métodos Se analizan prospectivamente los datos de 2.416 pacientes consecutivos hospitalizados por SCA en un hospital terciario (Islas Canarias, España), desde diciembre de 2012 hasta diciembre de 2017. La Red Europea de Calidad del Aire midió las concentraciones de material particulado de diámetro aerodinámico <10 μm (PM10) y gases reactivos. Se aplicó un diseño mediante estratificación en el tiempo de casos cruzados, utilizando modelos de regresión condicional de Poisson, para estimar el impacto de los eventos de polvo sahariano de PM10 en la incidencia de SCA. Resultados Los eventos de polvo sahariano observados los días 0 a 5 tras el inicio del SCA no mostraron asociación significativa con la incidencia de SCA. Los cocientes de tasas de incidencia de las concentraciones de PM10 1, 2, 3, 4 y 5 días antes del inicio del SCA (para cambios de 10 μg/m3) fueron 1,27 (IC95%, 0,87-1,85), 0,92 (IC95%, 0,84-1,01), 0,74 (IC95%, 0,45-1,22), 0,98 (IC95%, 0,87-1,11) y 0,95 (IC95%, 0,84-1,06). Conclusiones Es poco probable que la exposición a polvo sahariano tenga relación con la incidencia de SCA. (AU)

Introduction and objectives Asian desert dust has recently been recognized as a trigger for acute myocardial infarction. The inflow of dust from the Sahara into Spain impairs air quality due to an increase in particulate matter concentrations in the ambient air. The aim of the present study was to elucidate whether Saharan dust events are associated with the incidence of acute coronary syndrome (ACS) in patients living near North Africa, the major global dust source. Methods We prospectively collected data on hospitalizations due to ACS in 2416 consecutive patients from a tertiary care hospital (Canary Islands, Spain) from December 2012 to December 2017. Concentrations of particulate matter with an aerodynamic diameter 10 microns or smaller (PM10) and reactive gases were measured in the European Air Quality Network implemented in the Canary Islands. We applied the time-stratified case crossover design using conditional Poisson regression models to estimate the impact of PM10 Saharan dust events on the incidence of ACS. Results The occurrence of Saharan dust events observed 0 to 5 days before the onset of ACS was not significantly associated with the incidence of ACS. Incidence rate ratios (IRR) of PM10 levels 1, 2, 3, 4 and 5 days before ACS onset (for changes in 10μg/m3) were 1.27 (95%CI, 0.87-1.85), 0.92 (95%CI, 0.84-1.01), 0.74 (95%CI, 0.45-1.22), 0.98 (95%CI, 0.87-1.11), and 0.95 (95%CI, 0.84-1.06), respectively. Conclusions Exposure to Saharan desert dust is unlikely to be associated with the incidence of ACS. (AU)

Fisiopatología de la enfermedad cardiovascular en pacientes con COVID-19. Isquemia, trombosis y disfunción cardiaca / Physiopathology of cardiovascular disease in patients with COVID-19. Ischemia, thrombosis and heart failure

Las complicaciones cardiovasculares tienen una alta prevalencia en los pacientes con COVID-19 y son motivo frecuente de hospitalización, mortalidad y secuelas. En está revisión se describen los principales mecanismos fisiopatológicos implicados en la aparición de estas complicaciones. Tras la viremia inicial, se produce una infiltración y reproducción en los pulmónes, con activación del sistema inmunitario, liberación de citocinas y generación de un estado proinflamatorio con sepsis y fallo multiorgánico. El daño miocárdico puede deberse a una afección viral directa con respuesta inflamatoria local, o indirectamente a una inflamación sistémica inapropiada con marcada liberación de citocinas. Además, se genera un estado protrombótico que, junto con la afección viral vascular, pueden desencadenar eventos trombóticos e isquémicos secundarios a daño microvascular o inestabilización de placas de ateroma previas. Son necesarios nuevos estudios para esclarecer la fisiopatología tras estos eventos cardiovasculares y contribuir al desarrollo de nuevos tratamientos efectivos

Cardiovascular complications are highly prevalent in patients with COVID-19 and frequently lead to hospitalization, death and long-term morbidity. This article describes the principle pathophysiological mechanisms involved in the development of these complications. After the initial viremia, viralinvasión and replication occurs in the lungs, accompanied by immune system activation, cytokine release and the induction of a proinflammatory state, with sepsis and multiorgan failure. Myocardial injury could be due to the direct effect of viralinvasión and a local inflammatory response or to the indirect effect of inappropriate systemic inflammation involving a cytokine storm. Furthermore, the development of a prothrombotic state, together with vascular disease due to the virus, could trigger ischemic and thrombotic events secondary to microvascular damage or to the destabilization of pre-existing atheromatous plaque. New research is needed to reveal the pathophysiological mechanisms underlying these cardiovascular events and to support the development of effective new treatments