Background: Remnant cholesterol (RC) is an emerging factor contributing to residual risk for the development of atherosclerotic cardiovascular disease (ASCVD). We aimed to investigate the association of RC with ASCVD in high ASCVD risk patients. Methods: RC was calculated in 906 participants (178 low/moderate-risk and 728 high-risk) consecutively recruited from a vascular registry. Subclinical carotid atherosclerosis was assessed by B-mode carotid ultrasonography. Maximal carotid wall thickness (maxWT) and carotid atherosclerotic burden (n >= 2 atherosclerotic plaques) were set as the vascular outcomes. An independent cohort of 87 consecutively recruited high-risk patients who were followed for their lipid profile for 3 months was also analyzed. Results: RC was increased in the high-risk group as compared to controls (26 +/- 17 vs. 21 +/- 11 mg/dl, respectively, p < 0.001). Increased RC levels were independently associated with increased maxWT and carotid atherosclerotic burden (p < 0.05), after adjustment for traditional cardiovascular risk factors (TRF) and ASCVD. RC levels were associated with the presence of flow-limiting ASCVD and coronary artery disease (CAD) (p < 0.05), after adjustment for TRFs. These associations remained significant in those not receiving hypolipidemic treatment and in treated individuals achieving LDL-C<10 0 mg/dl. In the prospective cohort, there was no significant interaction between change in RC levels and hypolipidemic status, as contrasted to LDL-C levels (p < 0.001). Conclusion: In a high-risk population, RC was associated with subclinical and clinically overt ASCVD, particularly in patients with the most adverse lipid phenotype (untreated) or in treated patients with a low LDL-related risk profile. These findings support a residual pro-atherosclerotic role of RC in high-risk patients. (c) 2022 Hellenic Society of Cardiology. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
A 64-year-old man with ischaemic cardiomyopathy, cardiac resynchronization therapy with defibrillator and previous ventricular tachycardia (VT) ablation presented due to electrical storm (ES) and recurrent discharges from the device. He was under mexiletine and carvedilol, as he discontinued amiodarone due to thyrotoxicosis. Intravenous esmolol and xylocaine, reprogramming of the device and general anaesthesia mildly reduced VT episodes and shocks. Left stellate ganglion blockade (LSGB) with continuous infusion of 0.2% ropivacaine terminated ES without completely ending VT events (five episodes in following 7 days). Considering the response to LSGB, cryoneurolysis (CRYO-S Painless, Metrum) of the left stellate ganglion (LSG) was attempted with ultrasound guidance to achieve long-term autonomic modulation (Figure). The needle was inserted at the C6 level to reach the prevertebral fascia on the top of Longus Colli muscle and one cryoapplication of 3 min was delivered (−78°C). No procedural complications were observed except transient Horner syndrome. Patient...
Background Radiofrequency catheter ablation remains the most effective management option for atrioventricular nodal reentry tachycardia (AVNRT). The risk of atrioventricular (AV) block requiring permanent pacemaker is substantial, but, currently, a reliable method to predict this complication is lacking. Methods The electrophysiologic studies (EPS) and baseline characteristics of patients who underwent catheter ablation for the treatment of AVNRT were retrospectively analyzed to investigate predisposing factors for AV block after treatment. Patients were followed for AV block at one month and one year after hospital discharge. Results Among 784 patients treated with catheter ablation for AVNRT between 1999 to 2019, 15 developed AV block. Patients with AV block were older (p = .001). Among the recorded EPS parameters, patients with AV block had significantly higher Atrial His interval (120 vs. 110 ms, p = .049), Wenckebach cycle length (WCL) (400 vs. 353 ms, p < .001) and tachycardia CL (400 vs. 387 ms, P = .01) during the ablation compared to their peers without AV block. Additionally, only WCL (OR = 1.1, 95% CI 1.02-1.19, p = .017) remained significant after adjustment for age, gender, ERP, AH interval, and HR. This association was confirmed by comparing patients with (n = 15) and without (n = 15) AV block using propensity score-matching. A WCL >= 400ms was associated with a 4-fold higher incidence of AV block (4.79% vs. 1.25%). Conclusion Increased pre-procedural WCL was associated with a high risk for AV block after catheter ablation treatment for AVNRT. These findings suggest that this readily available EPS-derived parameter may be a novel marker of risk for severe complications in these patients.
COVID-19 infection is a new disease mainly affecting the respiratory system but is also accompanied by many extra-pulmonary manifestations. A case of a 47-year old male with unique myocardial fibrosis after COVID-19 infection involving the left ventricular wall, intraventricular septum and almost complete damage of interatrial septum, in combination with asymptomatic severe sinus arrest episodes related to mild obstructive sleep apnea syndrome is described here.
ABSTRACT:COVID-19 pandemic caused a major crisis, affecting and straining health care systems, including some very advanced ones. The pandemic may have also indirectly affected access to health care for patients with other conditions, not related to COVID-19, even in countries not overwhelmed by an outbreak.We analyzed and compared visits to the emergency room (ER) department during the same calendar period of 2019 and 2020 (from March 1 to March 31 of each year) in our hospital, a medium size, tertiary center, located in the center of Athens, which is not a referral center for COVID-19.Total ER visits were reduced by 42.3% and the number of those requiring hospitalization by 34.8%. This reduction was driven by lower numbers of visits for low risk, non-specific symptoms and causes. However, there was a significant decrease in admissions for cardiovascular symptoms and complications (chest pain of cardiac origin, acute coronary syndromes, and stroke) by 39.7% and for suspected or confirmed GI hemorrhage by 54.7%. Importantly, number of ER visits for infections remained unchanged, as well as the number of patients that required hospitalization for infection management; only few patients were diagnosed with COVID-19.During the initial period of the pandemic and lock-down in Greece, there was a major decrease in the patients visiting ER department, including decrease in the numbers of admissions for cardiovascular symptoms and complications. These observations may have implications for the management of non-COVID-19 diseases during the pandemic.
SARS-CoV-2 (Covid-19) infection has recently become a worldwide challenge with dramatic global economic and health consequences. As the pandemic is still spreading, new data concerning Covid-19 complications and related mechanisms become increasingly available. Accumulating data suggest that the incidence of cardiac arrest and its outcome are adversely affected during the Covid-19 period. This may be further exacerbated by drug-related cardiac toxicity of Covid-19 treatment regimens. Elucidating the underlying mechanisms that lead to Covid-19 associated cardiac arrest is imperative, not only in order to improve its effective management but also to maximize preventive measures. Herein we discuss available epidemiological data on cardiac arrest during the Covid-19 pandemic as well as possible associated causes and pathophysiological mechanisms and highlight gaps in evidence warranting further investigation. The risk of transmission during cardiopulmonary resuscitation (CPR) is also discussed in this review. Finally, we summarize currently recommended guidelines on CPR for Covid-19 patients including CPR in patients with cardiac arrest due to suspected drug-related cardiac toxicity in an effort to underscore the most important common points and discuss discrepancies proposed by established international societies.
SARS-CoV-2 (Covid-19) infection has recently become a worldwide challenge with dramatic global economic and health consequences As the pandemic is still spreading, new data concerning Covid-19 complications and related mechanisms become increasingly available Accumulating data suggest that the incidence of cardiac arrest and its outcome are adversely affected during the Covid-19 period This may be further exacerbated by drug-related cardiac toxicity of Covid-19 treatment regimens Elucidating the underlying mechanisms that lead to Covid-19 associated cardiac arrest is imperative, not only in order to improve its effective management but also to maximize preventive measures Herein we discuss available epidemiological data on cardiac arrest during the Covid-19 pandemic as well as possible associated causes and pathophysiological mechanisms and highlight gaps in evidence warranting further investigation The risk of transmission during cardiopulmonary resuscitation (CPR) is also discussed in this review Finally, we summarize currently recommended guidelines on CPR for Covid-19 patients including CPR in patients with cardiac arrest due to suspected drug-related cardiac toxicity in an effort to underscore the most important common points and discuss discrepancies proposed by established international societies
Incidence of atrial fibrillation (AF) during pregnancy is expected to increase in parallel to the increased mean age of conception and the percentage of pregnant women with congenital or structural heart disease. Cases of AF in pregnant women should be managed by an experienced cardiologist or an electrophysiologist. In terms of treatment options, direct cardioversion is highly effective and safe in pregnancy. Therefore, it should be preferred over pharmacologic cardioversion with intravenous ibutilide or flecainide. In contrast, amiodarone is not recommended. In respect to rate-control pharmaceutic agents, beta-blockers (except for atenolol) and digoxin should be considered as the first treatment option with the widest experience of use. Interventional techniques are usually deferred after the end of pregnancy; however, catheter ablation could be offered in selected cases of atrial flutter refractory to medication, preferably during the second trimester. To this end, fluoroless techniques must be employed. Finally, vitamin K antagonists (VKAs) are recommended after the first trimester whilst non-VKA oral anticoagulants should be avoided given the limited experience in this special population. Low molecular weight heparin is an acceptable and effective treatment for anticoagulation but periodic evaluation of anti-Xa factor is warranted. Of note, tools currently used for prediction of stroke risk in non-pregnant patients with AF have not been validated in pregnancy. Overall, treatment of AF in pregnancy must be balanced between expected benefit and potential harm and constantly updated according to mother's symptoms, fetus' signs and clinical response. Further studies are needed to evaluate optimal therapeutic strategies for supraventricular arrhythmias in pregnancy.
A 60-year-old patient presented with recalcitrant electrical storm (ES). Mild sedation and initial antiarrhythmic combination of esmolol and amiodarone did not affect the intensity of ES, which resulted in battery exhaustion. Oral propranolol in addition to intravenous amiodarone might be preferred in hemodynamically stable patients before interventional therapies. (Level of Difficulty: Intermediate.)
Purpose of Review Electrical storm (ES) is a life-threatening medical emergency of repetitive episodes of sustained ventricular arrhythmias within a short period. Its occurrence is associated with poor short- and long-term survival, even in patients with implantable cardioverter defibrillators (ICD). Management of ES is challenging and mainly based on retrospective studies. This article reviews the existing literature on ES, presents the available data regarding its management, and proposes a new algorithm based on current evidence. Recent Findings Recent research could modify the management of ES supporting the role of non-selective β1 and β2 blockade and the early intervention with catheter ablation as well as strengthening the role of cardiac sympathetic denervation. Summary A multipronged approach should be considered for the management of ES including identification and correction of reversible causes, ICD reprogramming, drug therapy (beta-blockers—especially non-selective ones—and other anti-arrhythmic drugs) and non-pharmacologic therapies such as catheter ablation and techniques of neuroaxial modulation. Although current data suggest early aggressive management, further research is required to clarify the optimal order and combination of therapies for the prevention of future events.
BACKGROUND:Lipid-lowering therapy and control of cardiovascular risk factors are the current recommendations of atherosclerotic disease management. Despite optimal treatment the rate of acute coronary syndrome events remains high. Inflammation plays an essential role in the pathophysiology of atherosclerotic plaque formation, progression and rupture, which conclusively causes acute clinical episodes. OBJECTIVE:This review aims to give a conceptual description of the potential therapeutic benefits and effects of colchicine in inflammation-mediated atherosclerotic disease and hypertriglyceridemia. METHOD:A complete literature survey was performed using the PubMed database search to collect available information regarding colchicine, atherosclerosis, and hypertriglyceridemia. RESULTS:A total of 42 studies met the selection criteria for inclusion in the review. Inflammation is a well-known key mediator of atherogenesis in coronary artery disease. Colchicine has direct antiinflammatory effects by inhibiting critical inflammatory signaling networks as the inflammasome, pro-inflammatory cytokines, and expression of adhesion molecules, preventing both local chemoattraction of inflammatory cells such as neutrophils and systemic inflammation including the decrease of the release of IL-1β by the neutrophils. CONCLUSION:Colchicine reduces the levels of inflammatory markers, stabilizes the coronary plaque, leads to more favorable cardiac healing after damage, and reduces the acute coronary syndromes event recurrence. Colchicine reduces the myocardial infarct size, myocardial fibrosis, and improves the hemodynamic parameters. Several studies report the potential attenuating role of colchicine on triglyceride levels. Current evidence though regarding the pathophysiological mechanism of colchicine's triglyceride-lowering effect remains scarce.
BACKGROUND Electrical storm (ES), characterized by unrelenting recurrences of ventricular arrhythmias, is observed in approximately 30% of patients with implantable cardioverter-defibrillators (ICDs) and is associated with high mortality rates. OBJECTIVES Sympathetic blockade with beta-blockers, usually in combination with intravenous (IV) amiodarone, have proved highly effective in the suppression of ES. In this study, we compared the efficacy of a nonselective beta-blocker (propranolol) versus a beta(1)-selective blocker (metoprolol) in the management of ES. METHODS Between 2011 and 2016, 60 ICD patients (45 men, mean age 65.0 +/- 8.5 years) with ES developed within 24 h from admission were randomly assigned to therapy with either propranolol (160 mg/24 h, Group A) or metoprolol (200 mg/24 h, Group B), combined with IV amiodarone for 48 h. RESULTS Patients under propranolol therapy in comparison with metoprolol-treated individuals presented a 2.67 times decreased incidence rate (incidence rate ratio: 0.375; 95% confidence interval: 0.207 to 0.678; p = 0.001) of ventricular arrhythmic events (tachycardia or fibrillation) and a 2.34 times decreased rate of ICD discharges (incidence rate ratio: 0.428; 95% CI: 0.227 to 0.892; p = 0.004) during the intensive care unit (ICU) stay, after adjusting for age, sex, ejection fraction, New York Heart Association functional class, heart failure type, arrhythmia type, and arrhythmic events before ICU admission. At the end of the first 24-h treatment period, 27 of 30 (90.0%) patients in group A, while only 16 of 30 (53.3%) patients in group B were free of arrhythmic events (p = 0.03). The termination of arrhythmic events was 77.5% less likely in Group B compared with Group A (hazard ratio: 0.225; 95% CI: 0.112 to 0.453; p < 0.001). Time to arrhythmia termination and length of hospital stay were significantly shorter in the propranolol group (p < 0.05 for both). CONCLUSIONS The combination of IV amiodarone and oral propranolol is safe, effective, and superior to the combination of IV amiodarone and oral metoprolol in the management of ES in ICD patients. (C) 2018 by the American College of Cardiology Foundation.
The failing myocardium is characterized by numerous inter-related perturbations at molecular, cell and tissue level. Notably, aged myocardium and heart failure (HF) share common pathophysiologic processes and accumulating evidence suggests that impairment of sympathetic nervous system may modulate the clinical course of both entities. Within the sympathetic nervous system, adrenergic receptors (ARs) and changes in regulation of their responses are considered the connecting link for both aging and cardiovascular disease. In particular, decreased β-AR responsiveness, increased circulating catecholamines, and overall hyposensitivity to adrenergic stress are common pathophysiologic derangements in cardiovascular aging and HF [1]. We have previously shown that oral propranolol is more efficient and faster than metoprolol in the treatment of patients with implantable cardioverter-defibrillator (ICD) who experience an electrical storm (ES). This was the first study to compare the efficacy of a nonselective (propranolol) versus a selective β-blocker (metoprolol) towards the management of complex ventricular arrhythmias in HF patients [2]. It is well known that the failing human heart activates compensatory mechanisms, among which increased sympathetic activity has a key role on effector signaling and downstream targets. Adrenergic receptors are divided in two classes: α and β. In terms of β-ΑRs, β1AR is primarily located in the myocardium while β2AR is widely distributed in multiple tissues and β3-AR is found in adipose tissue [3]. As further explained in the specific study, failing myocardium exhibits a progressive decrease in β1/β2 ratio that is attributed to selective down regulation of the β1 receptors. Propranolol may effectively block signal transductions from both β1 and -unblocked from metoprololupregulated β2 cardiac receptors. Given that HF patients are also characterized by increased age, it is tempting to speculate that the combined effect of myocardium disease and aging inflates β-AR stimulation and ES represents an extreme form of sympathetic overdrive that necessitates a more potent β-blocker for prompt and successful treatment. Along this line, protein kinase A (PKA) is an important mediator of signal transduction downstream of G-protein coupled receptors in response to cAMP. Protein kinase A is comprised of two regulatory subunits, RI and RII. As PKA (and in specific, RIIβ) declines with aging, the β-adrenergic pathEditorial
We read with great interest the editorial article “ Electrical storm: mechanistic and therapeutic considerations to avoid death in the survivors ” by Tsuji and Dobrev which brings into spotlight mitochondria as an emerging and significant determinant of heart failure (HF) outcome. Despite the fact that current treatments for HF as well as electrical storm treatment do not directly target mitochondria, it would be interesting to approach their effects on them, with focus on β-adrenergic signaling.
Cardiac management devices have become an integral part of our armament for treatment of heart diseases. However, complications may arise that mandate extraction of either the device or the lead. The noninterventional lead extraction has become a topic of avid debate as simple traction is associated with low success rates whereas laser-assisted extraction carries a high economic cost. Herein we present a case of 22-year-old pacemaker leads extracted with a novel "trouserslike technique" that could present an attractive alternative for leads implanted for more than 10 years when laser sheaths are not accessible.
Objective: Associations of endogenous androgens in menopause with blood pressure (BP) and indices of arterial stiffness are reported, but directional relationships are not clear. Structural equation modeling is a contemporary statistical method, which allows assessment of such relationships and improves pathway understanding. Methods: We recruited 411 consecutive apparently healthy postmenopausal women who underwent noninvasive vascular evaluation. This included pulse wave analysis (aortic pressures and arterial wave reflections [augmentation index]), measurement of aortic stiffness by pulse wave velocity (PWV), stiffness index (SI), and flow-mediated dilatation. A cumulative marker combining PWV and SI (combined local and aortic arterial stiffness [CAS]) was also assessed. Free androgen index (FAI) was calculated from circulating total testosterone and sex hormone-binding globulin. Results: FAI was an independent determinant of systolic BP (SBP) (P = 0.032), SI (P = 0.042), and PWV (P = 0.027). Under structural equation modeling analysis, FAI was a direct predictor for PWV (beta = 0.149, P = 0.014), SI (beta = 0.154, P = 0.022), and CAS (beta = 0.193, P = 0.02), whereas SBP was a parallel mediator of androgen's vascular effects on PWV (beta = 0.280, P < 0.001) and CAS (beta = 0.248, P = 0.004), but not SI (beta = 0.024, P = 0.404). FAI-induced increase in arterial stiffness via flow-mediated dilatation was not established. FAI was not a determinant of augmentation index. Conclusions: In healthy postmenopausal women, FAI was directly associated with PWV, SI, and CAS. FAI also directly correlated with SBP, which in turn concurrently increased PWV and CAS. The directional correlations found herein, imply that endogenous androgens may be causally associated with indices of arterial stiffness both directly and indirectly. This hypothesis should be confirmed in further studies with causal design.
Early repolarization syndrome ( ERS ) was originally considered a normal variant with benign outcome. However, recent studies have demonstrated that it can be linked to a considerable risk of life‐threatening arrhythmias and sudden cardiac death. We report a case with an extraordinary, extremely malignant clinical expression of ERS refractory to all antiarrhythmic drugs including quinidine. This case demonstrates real‐time changes of dynamic electrocardiogram ( ECG ) preceding a polymorphic ventricular tachycardia ( VT )‐ventricular fibrillation ( VF ) and possible external factors triggering arrhythmia onset. Implantable cardioverter‐defibrillator ( ICD ) function was terminated 6 months after implantation due to multiple‐incessant electrical storm ( ES ). Catheter ablation was the definite treatment of this malignant entity.
Although long-term weight gain has been associated with cardiovascular risk and intima-media thickening (IMT), no sufficient data exist on possible associations of such weight changes with more advanced stages of subclinical atherosclerosis. Moreover, the value of self-reported weight changes, a more practical approach to assess long-term history in adiposity status, is still a matter of debate. In this longitudinal study, long-term changes in BMI and overweight status were assessed in 106 healthy young adults (age 40.5 +/- 1.1 years, 60 males). These were a subgroup of adolescent school students who had originally been examined in 1983 initially aiming to assess cardiovascular risk factor prevalence. Markers of early (carotid IMT) and advanced (presence of plaques in the carotid and femoral arteries and ankle-brachial index, ABI) subclinical atherosclerosis were measured in all individuals. By multivariate analysis, among other risk factors, IMT and the presence of plaques were independently determined by BMI change, while a low ABI was also determined by changes in overweight status. An adverse long term adiposity profile change (>= +4 kg/m(2) and/or change into overweight/obese status from normal weight since adolescence) incrementally determined a low ABI over current risk factors. Self-reported and actual BMI changes were correlated (r = 0.587) but their means significantly differed, while the former significantly correlated with IMT only (P = 0.032). In conclusion, an adverse long term adiposity status change was more prominently associated with advanced subclinical atherosclerosis and particularly low ABI. These results also suggest that the utility of self-reported weight changes may be limited in primary prevention practice.