Mortality decline in women to a lesser extent than in men with coronary artery disease (CAD) has provoked a bigger interest in some already existing dilemmas and questions. Many studies carried out ...in the past three decades did not provide us with precise conclusions. Moreover, various challenges in the prevention, diagnosis, treatment and outcome of CAD in women are still remaining. The meta-analysis and the systematic review conducted in the last years have offered novel approaches to understanding CAD gender disparities in access to care and coronary disease management in women, but women are more likely to experience less favorable short- and long-term outcomes than men do. The reasons for these findings should lie in several known segments in the CAD pathophysiological mechanisms different in women and ultimately leading to a lower quality of care. Clinical presentation in women, which is often characterized by atypical chest pain and a higher prevalence of non-obstructive CAD when evaluated invasively, places women to the false-negative diagnosis of CAD and influences inadequate access to care. Clinical presentation and diagnostic methods, as well as the appropriate treatment options insufficiently examined in women, need to be better defined. The traditional CAD risk factors have a greater impact on women than on men. Unique CAD risk factors only seen in women, have recently been recognized with more attention. However, it is important to note that even in women with obstructive CAD and typical clinical presentation, invasive therapy and pharmacologic therapy are not always implemented as recommended by guidelines as in men. Women are underrepresented in CAD trials, and in current guidelines, gender differences in CAD management have not yet been justified. The underestimation of the risk of CAD in women, followed by its underdiagnosis and undertreatment, might be one of the reasons for a worse prognosis in women in comparison with men.
Although disturbance of redox homeostasis might be responsible for COVID-19 cardiac complications, this molecular mechanism has not been addressed yet. We have proposed modifying the effects of ...antioxidant proteins polymorphisms (superoxide dismutase 2 (
), glutathione peroxidase 1 (
), glutathione peroxidase 3 (
) and nuclear factor erythroid 2-related factor 2, (
)) in individual susceptibility towards the development of cardiac manifestations of long COVID-19. The presence of subclinical cardiac dysfunction was assessed via echocardiography and cardiac magnetic resonance imaging in 174 convalescent COVID-19 patients. SOD2,
,
and
polymorphisms were determined via the appropriate PCR methods. No significant association of the investigated polymorphisms with the risk of arrhythmia development was found. However, the carriers of variant
*T,
*C or
*A alleles were more than twice less prone for dyspnea development in comparison with the carriers of the referent ones. These findings were even more potentiated in the carriers of any two variant alleles of these genes (OR = 0.273, and
= 0.016). The variant
alleles were significantly associated with left atrial and right ventricular echocardiographic parameters, specifically LAVI, RFAC and RV-EF (
= 0.025,
= 0.009, and
= 0.007, respectively). Based on the relation between the variant
*T allele and higher levels of LV echocardiographic parameters, EDD, LVMI and GLS, as well as troponin T (
= 0.038), it can be proposed that recovered COVID-19 patients, who are the carriers of this genetic variant, might have subtle left ventricular systolic dysfunction. No significant association between the investigated polymorphisms and cardiac disfunction was observed when cardiac magnetic resonance imaging was performed. Our results on the association between antioxidant genetic variants and long COVID cardiological manifestations highlight the involvement of genetic propensity in both acute and long COVID clinical manifestations.
Objective. The objective of this study is to analyze the impact of declining kidney function on the occurrence of the slow-flow/no-reflow phenomenon in patients with ST-elevation myocardial ...infarction (STEMI) treated with primary PCI (pPCI), as well as the analysis of the prognostic impact of the slow-flow/no-reflow phenomenon on short- and long-term mortality in these patients. Methods. We analyzed 3,115 consecutive patients. A value of the glomerular filtration rate (eGFR) at the time of admission of eGFR <90 ml/min/m2 was considered a low baseline eGFR. The follow-up period was 8 years. Results. The slow-flow/no-reflow phenomenon through the IRA was registered in 146 (4.7%) patients. Estimated GFR of <90 ml/min/m2 was an independent predictor for the occurrence of the slow-flow/no-reflow phenomenon (OR 2.91, 95% CI 1.25–3.95, p < 0.001), and the risk for the occurrence of the slow-flow/no-reflow phenomenon increased with the decline of the kidney function: eGFR 60–89 ml/min/m2: OR 1.94 (95% CI 1.22–3.07, p = 0.005), eGFR 45–59 ml/min/m2: OR 2.55 (95% CI 1.55–4.94, p < 0.001), eGFR 30–44 ml/min/m2: OR 2.77 (95% CI 1.43–5.25, p < 0.001), eGFR 15–29 ml/min/m2: OR 5.84 (95% CI 2.84–8.01, p < 0.001). The slow-flow/no-reflow phenomenon was a strong independent predictor of short- and long-term all-cause mortality: 30-day mortality (HR 2.62, 95% CI 1.78–3.57, p < 0.001) and 8-year mortality (HR 2.09, 95% CI 1.49–2.09, p < 0.001). Conclusion. Reduced baseline kidney function was an independent predictor for the occurrence of the slow-flow/no-reflow phenomenon, and its prognostic impact started with the mildest decrease in eGFR (below 90 ml/min/m2) and increased with its further decline. The slow-flow/no-reflow phenomenon was a strong independent predictor of mortality in the short- and long-term follow-up of the analyzed patients.
Background/Aim. The prognostic impact of complete atrioventricular (AV) block on the long-term prognosis of patients with ST-elevation myocardial infarction (STEMI) has not been fully determined. The ...aim of the study was to analyze the incidence and prognostic impact of complete AV block on in-hospital mortality (IHM) and 6-year mortality in STEMI patients treated with primary percutaneous coronary intervention. Methods. The study included 3,044 consecutive STEMI patients. Results. Complete AV block was registered only on admission in 144 (4.73%) patients; 125 (86.8%) patients with complete AV block had inferior infarction. A temporary pacemaker was implanted in 72 (50%) patients with complete AV block. No patient under-went permanent pacemaker implantation. IHM was significantly higher in patients with complete AV block than in patients without complete A V b lock: 1 7.9% v s. 3 .6%, respectively, p < 0.001. In patients with heart block and inferior infarction, IHM was 13%, whereas IHM was 53% in patients with heart block and anterior infarction. When we analyzed patients discharged alive from the hospital, we also found a significantly higher long-term (6-year) mortality rate in those with complete AV block vs. patients without AV block: 7.8% vs. 3.4%, respectively, p < 0.001. Complete AV block was an independent predictor for IHM and 6-year mortality: IHM odds ratio (OR) 2.94 95%, confidence interval (CI) 1.23?5.22; 6-year mortality hazard ratio (HR) 1.61, 95%, CI 1.10?2.37. When subanalysis was performed in patients with inferior STEMI, complete AV block was an independent predictor of IHM and 6 -year mortality, while in patients with anterior STEMI, complete AV block was an independent predictor of IHM. Conclusion. In analyzed STEMI patients, complete AV block was transitory and was registered only on hospital admission. Although transitory, complete AV block remained a strong independent predictor of IHM and long-term mortality.
OBJECTIVEIn this study, we aimed to examine the prognostic impact of decreased kidney function at admission on the occurrence of new-onset atrial fibrillation (AF) in patients with ST-elevation ...myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). METHODSThe study enrolled 3,115 consecutive patients with STEMI. Kidney function was assessed by estimation of the glomerular filtration rate (eGFR) at admission. Patients with cardiogenic shock at admission, patients on hemodialysis, and patients with a medical history of previous AF (paroxysmal, persistent, or permanent) were excluded. The follow-up period was six years. RESULTSNew-onset AF occurred in 215 (6.9%) patients, 75 (34.9%) patients presented with AF, and 140 (65.1%) patients developed AF after pPCI. The median time of AF occurrence in patients who did not present with AF was 4.5 (interquartile range 1-25) hours after pPCI. New-onset AF was associated with a higher short- and long-term mortality. In the multiple logistic regression analysis, all stages of reduced kidney function were independent predictors for the occurrence of new-onset AF, and negative prognostic impact increased with the deterioration of kidney function: eGFR <90 mL/min/m2, hazard ratio (HR) 1.96, 95% confidence interval (CI) 1.42-2.89, p=0.011; eGFR 60-89 mL/min/m2, HR 1.54, 95% CI 1.13-2.57, p=0.045; eGFR 45-59 mL/min/m2-, HR 2.09, 95% CI 1.24-2.85, p=0.023; eGFR 30-44 mL/min/m2-, HR 2.93, 95% CI 1.64-5.29, p<0.001; eGFR 15-29 mL/min/m2-, HR 5.51, 95% CI 2.67-11.39, p<0.001. CONCLUSIONDecreased kidney function was significantly associated with the occurrence of new-onset AF, and its impact increased with the deterioration in kidney function, starting with an eGFR value of 90 mL/min/m2. New-onset AF was an independent predictor of long-term all-cause mortality in the analyzed patients.
Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome that is often overlooked, misdiagnosed, and maltreated. Medical treatment poses a significant challenge ...because of the lack of randomized studies to guide treatment. The initial clinical presentation should guide medical and interventional management. Fibrinolytic agents and anticoagulants should be avoided because they could favor hematoma propagation. In patients with SCAD, antiplatelet therapy should be prescribed especially dual antiplatelet therapy (DAPT) consisting of aspirin and clopidogrel, whereas potent P2Y12 inhibitors, e.g., ticagrelor and prasugrel, should be avoided. If a stent was used, DAPT should be continued for 12 months. Aspirin only can be an option for patients without “high-risk” angiographic features—thrombus burden, critical stenosis, and decreased coronary flow. Beta-blocking (BB) agents should be used to prevent recurrence of SCAD. There is a general agreement that angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, mineralocorticoid antagonists, and loop diuretics should be used in patients with SCAD experiencing the symptoms of heart failure and a decrease in left ventricular ejection fraction below 50%. Although without firm evidence, statins can be used in SCAD due to their pleiotropic properties. The results of a randomized trial on the use of BB and statins are awaited. Aggregation of data from national registries might point out truly beneficial medications for patients with SCAD.
Background: stress hyperglicemia (SH) is common in patients with ST-elevation myocardial infraction (STEMI). The aims of this study were to analyze the impact of SH on the incidence of all-cause ...mortality and major adverse cardiovascular events (MACE-cardiovascular death, nonfatal reinfarction, target vessel revascularization, and stroke) in STEMI patients without diabetes mellitus (DM) who have been treated successfully with primary PCI (pPCI). Method: we analyzed 2362 STEMI patients treated with successful pPCI (post-procedural flow TIMI = 3) and without DM and cardiogenic shock at admission. Stress hyperglycemia was defined as plasma glucose level above 7.8 mmol/L at admission. The follow-up period was 8 years. Results: incidence of SH was 26.9%. Eight-year all-cause mortality and MACE rates were significantly higher in patients with SH, as compared to patients without SH (9.7% vs. 4.2%, p < 0.001, and 15.7% vs. 9.4%, p < 0.001). SH was an independent predictor of short- and long-term all-cause mortality (HR 2.19, 95%CI 1.16–4.18, and HR 1.99, 95%CI 1.03–3.85) and MACE (HR 1.49, 95%CI 1.03–2.03, and HR 1.35, 95%CI 1.03–1.89). Conclusion: despite successful revascularization, SH at admission was an independent predictor of short-term and long-term (up to eight years) all-cause mortality and MACE, but its negative prognostic impact was stronger in short-term follow-up.
The aim of this retrospective study was to identify myocardial injury after COVID-19 inflammation and explore whether myocardial damage could be a possible cause of the persistent symptoms following ...COVID-19 infection in previously healthy individuals. This study included 139 patients who were enrolled between January and June 2021, with a mean age of 46.7 ± 15.2 years, of whom 68 were men and 71 were women without known cardiac or pulmonary diseases. All patients underwent clinical work-up, laboratory analysis, cardiac ultrasound, and CMR on a 1.5 T scanner using a recommended protocol for morphological and functional assessment before and after contrast media application with multi-parametric sequences. In 39% of patients, late gadolinium enhancement (LGE) was found as a sign of myocarditis. Fibrinogen was statistically significantly higher in patients with LGE than in those without LGE (4.3 ± 0.23 vs. 3.2 ± 0.14 g/L,
< 0.05, respectively), as well as D-dimer (1.8 ± 0.3 vs. 0.8 ± 0.1 mg/L FEU). Also, troponin was statistically significantly higher in patients with myocardial LGE (13.1 ± 0.4 ng/L) compared to those with normal myocardium (4.9 ± 0.3 ng/L,
< 0.001). We demonstrated chest pain, fatigue, and elevated troponin to be independent predictors for LGE. Septal LGE was shown to be a predictor for arrhythmias. The use of CMR is a potential risk stratification tool in evaluating outcomes following COVID-19 myocarditis.
Spontaneous coronary artery dissection (SCAD) accounts for 1.7%–4% of all acute coronary syndrome presentations, particularly among young women with an emerging awareness of its importance. The ...demarcation of acute SCAD from coronary atherothrombosis and the proper therapeutic approach still represents a major clinical challenge. Certain arteriopathies and triggers are related to SCAD, with high variability in their prevalence, and often, the cause remains unknown. The objective of this review is to provide contemporary knowledge of the pathophysiology of SCAD and possible therapeutic solutions.
A significant percentage of younger patients with myocardial infarction have premature coronary artery disease (CAD). The aims of this study were to analyze all-cause mortality and major adverse ...cardiovascular events (MACEs cardiovascular death, non-fatal reinfarction, stroke, target vessel revascularization) during eight-year follow-up in patients with ST-elevation myocardial infarction (STEMI) and premature CAD.
We analyzed 2560 STEMI patients without previous CAD and without cardiogenic shock at admission who were treated with primary PCI. CAD was classified as premature in men aged <50 years and women <55 years.
Premature CAD was found in 630 (24.6%) patients. Patients with premature CAD have fewer comorbidities and better initial angiographic findings compared to patients without premature CAD. The incidence of non-fatal adverse ischemic events was similar to the incidence in older patients. Premature CAD was an independent predictor for lower mortality (HR 0.50 95%CI 0.28-0.91) and MACEs (HR 0.27 95%CI 0.15-0.47). In patients with premature CAD, EF < 40% was the only independent predictor of mortality (HR 5.59 95%CI 2.18-8.52) and MACEs (HR 4.18, 95%CI 1.98-8.13).
Premature CAD was an independent predictor for lower mortality and MACEs. In patients with premature CAD, EF < 40% was an independent predictor of eight-year mortality and MACEs.
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