Role of Vitamins in Cardiovascular Health: Know Your Facts - Part 1.

Cardiovascular (CV) disease (CVD) is a major cause of morbidity and mortality world-wide, thus it is important to adopt preventive interventions. Observational data demonstrating CV benefits of vitamin supplements, advanced by self-proclaimed experts have resulted in ~50% of Americans reporting the use of multivitamins for health promotion; this practice has led to a multi-billion-dollar business of the multivitamin-industry. However, the data on the extensive use of multivitamins show no consistent benefit for CVD prevention or all-cause mortality, while the use of certain vitamins might prove harmful. Thus, the focus of this two-part review is on the attributes or concerns about specific vitamins on CVD. In Part 1, the CV effects of specific vitamins are discussed, indicating the need for further supportive evidence of potential benefits. Vitamin A preserves CV homeostasis as it participates in many biologic functions, including atherosclerosis. However, supplementation could potentially be harmful. Betacarotene, a pro-vitamin A, conveys pro-oxidant actions that may mitigate any other benefits. Folic acid alone and certain B-vitamins (e.g., B1/B2/B6/B12) may reduce CVD, heart failure, and/or stroke, while niacin might increase mortality. Vitamin C has antioxidant and cardioprotective effects. Vitamin D may confer CV protection, but all the data are not in agreement. Combined vitamin E and C have antiatherogenic effects but clinical evidence is inconsistent. Vitamin K seems neutral. Thus, there are individual vitamin actions with favorable CV impact (certain B-vitamins and vitamins C and D), but other vitamins (ß-carotene, niacin) may potentially have deleterious effects, which also holds true for high doses of fat-soluble vitamins (A/D/E/K).

Role of Vitamins in Cardiovascular Health: Know Your Facts-Part 2.

Cardiovascular disease (CVD) is a major cause of morbidity/mortality world-wide, hence preventive interventions are crucial. Observational data showing beneficial CV effects of vitamin supplements, promoted by self-proclaimed experts, have led to ~50% of Americans using multivitamins; this practice has culminated into a multi-billion-dollar business. However, robust evidence is lacking, and certain vitamins might incur harm. This two-part review focuses on the attributes or concerns about specific vitamin consumption on CVD. The evidence for indiscriminate use of multivitamins indicates no consistent CVD benefit. Specific vitamins and/or combinations are suggested, but further supportive evidence is needed. Data presented in Part 1 indicated that folic acid and certain B-vitamins may decrease stroke, whereas niacin might raise mortality; beta-carotene mediates pro-oxidant effects, which may abate the benefits from other vitamins. In Part 2, data favor the anti-oxidant effects of vitamin C and the anti-atherogenic effects of vitamins C and E, but clinical evidence is inconsistent. Vitamin D may provide CV protection, but data are conflicting. Vitamin K appears neutral. Thus, there are favorable CV effects of individual vitamins (C/D), but randomized/controlled data are lacking. An important caveat regards the potential toxicity of increased doses of fat-soluble vitamins (A/D/E/K). As emphasized in Part 1, vitamins might benefit subjects who are antioxidant-deficient or exposed to high levels of oxidative-stress (e.g., diabetics, smokers, and elderly), stressing the importance of targeting certain subgroups for optimal results. Finally, by promoting CV-healthy balanced-diets, we could acquire essential vitamins and nutrients and use supplements only for specific indications.

Depression and atrial fibrillation in a reciprocal liaison: a neuro-cardiac link.

OBJECTIVE: To explore the reciprocal relationship of depression and atrial fibrillation (AF). METHODS: A literature search was conducted in Pub Med, Scopus, and Google Scholar using relevant terms for depression and AF and respective therapies. RESULTS: There is evidence that depression is involved in the aetiology and prognosis of AF. AF, independently of its type, incurs a risk of depression in 20-40% of patients. Also, depression significantly increases cumulative incidence of AF (from 1.92% to 4.44% at 10 years); 25% increased risk of new-onset AF is reported in patients with depression, reaching 32% in recurrent depression. Hence, emphasis is put on the importance of assessing depression in the evaluation of AF and vice versa. Persistent vs paroxysmal AF patients may suffer from more severe depression. Furthermore, depression can impact the effectiveness of AF treatments, including pharmacotherapy, anticoagulation, cardioversion and catheter ablation. CONCLUSIONS: A reciprocal association of depression and AF, a neurocardiac link, has been suggested. Thus, strategies which can reduce depression may improve AF patients' course and treatment outcomes. Also, AF has a significant impact on risk of depression and quality of life. Hence, effective antiarrhythmic therapies may alleviate patients' depressive symptoms. KEY POINTSAF, independently of its type of paroxysmal, permanent or chronic, appears to have mental besides physical consequences, including depression and anxietyA reciprocal influence or bidirectional association of depression and AF, a neurocardiac link, has been suggestedAF has considerable impact on the risk of depression occurrence with 20-40% of patients with AF found to have high levels of depressionAlso, depression significantly increases 10-year cumulative incidence and risk of AF from 1.92% to 4.44% in people without depression, and the risk of new-onset AF by 25-32%Emphasis should be placed on the importance of assessing depression in the evaluation of AF and vice versaPersistent/chronic AF patients may suffer from more severe depressed mood than paroxysmal AF patients with similar symptom burdenDepression and anxiety can impact the effectiveness of certain AF treatments, including pharmacotherapy, anticoagulation treatment, cardioversion and catheter ablationThus, strategies which can reduce anxiety and depression may improve AF patients' course and treatment outcomesAlso, effective antiarrhythmic therapies to control AF may alleviate patients' depressive mood.

Features of a Balanced Healthy Diet with Cardiovascular and Other Benefits.

BACKGROUND: Cardiovascular (CV) disease (CVD) remains the leading cause of death globally. Besides lack of exercise, obesity, smoking, and other risk factors, poor nutrition and unhealthy/ unbalanced diets play an important role in CVD. OBJECTIVE: This review examined data on all issues of the CV-health benefits of a balanced diet, with tabulation of nutritional data and health-authority recommendations and pictorial illustration of the main features of a CV-healthy diet. METHODS: PubMed and Google Scholar were searched for relevant studies and reviews on diet and CV health. RESULTS: For a long time, there has been evidence, corroborated by recent findings, that pro-vegetarian diets have a beneficial influence on serum lipid levels, markers of inflammation and endothelial function, prooxidant-antioxidant balance, and gut microbiome, all probably contributing to reduced CV risk. Worries about the nutritional adequacy of vegetarian diets are circumvented by obtaining certain nutrients lacking or found in lower amounts in plants than in animal foods, by consuming a wide variety of healthy plant foods and through intake of oral supplements or fortified foods. Well-balanced diets, such as the Mediterranean or the Dietary-Approaches-to-Stop-Hypertension diets, provide CV-health benefits. Nevertheless, a broad variety of plant-based diets with low/minimal animal food intake may allow for a personalized and culturally adjusted application of dietary recommendations contributing to the maintenance of CV health. CONCLUSION: Universal adoption of a balanced CV-healthy diet can reduce global, CV and other mortality by ~20%. This requires world-wide programs of information for and education of the public, starting with school children and expanding to all groups, sectors, and levels.

Sodium-glucose cotransporter type 2 inhibitors and cardiac arrhythmias.

The introduction of sodium-glucose cotransporter 2 (SGLT2) inhibitors as a new and effective class of therapeutic agents for type 2 diabetes (T2D) preventing the reabsorption of glucose in the kidneys and thus facilitating glucose excretion in the urine, but also as agents with cardiovascular benefits, particularly in patients with heart failure (HF), regardless of the diabetic status, has ushered in a new era in treating patients with T2D and/or HF. In addition, data have recently emerged indicating an antiarrhythmic effect of the SGLT2 inhibitors in patients with and without diabetes. Prospective studies, randomized controlled trials and meta-analyses have provided robust evidence for a protective and beneficial effect of these agents against atrial fibrillation, ventricular arrhythmias and sudden cardiac death. The antiarrhythmic mechanisms involved include reverse atrial and ventricular remodeling, amelioration of mitochondrial function, reduction of hypoglycemic episodes with their attendant arrhythmogenic effects, attenuated sympathetic nervous system activity, regulation of sodium and calcium homeostasis, and suppression of prolonged ventricular repolarization. These new data on antiarrhythmic actions of SGLT2 inhibitors are herein reviewed, potential mechanisms involved are discussed and pictorially illustrated, and treatment results on specific arrhythmias are described and tabulated.

Takotsubo Syndrome and Sudden Cardiac Death.

Takotsubo syndrome (TTS), triggered by intense emotional or physical stress, occurring most commonly in post-menopausal women, presents as an ST-elevation myocardial infarction (MI). Cardiovascular complications occur in almost half the patients with TTS, and the inpatient mortality is comparable to MI (4-5%) owing to cardiogenic shock, myocardial rupture, or life-threatening arrhythmias. Thus, its prognosis is not as benign as previously thought, as it may cause mechanical complications (cardiac rupture) and potentially lethal arrhythmias and sudden cardiac death (SCD). Similar to MI, some patients may perish before reaching the hospital due to out-of-hospital cardiac arrest; this may lead to underestimation of the actual SCD risk. Furthermore, after discharge, some patients may develop late SCD and/or TTS recurrence that may result in SCD. There are risk factors for SCD in TTS patients, such as severe/persistent QT-interval prolongation inciting torsade-de-pointes, other ECG abnormalities (diffuse giant negative T-waves, widened QRS-complex), bradyarrhythmias, comorbidities, concurrent obstructive coronary artery disease or vasospasm, male gender, older age, severe left ventricular dysfunction, and use of sympathomimetic drugs. All these issues are herein reviewed, case reports/series and data from large cohort studies and meta-analyses are analyzed, risk factors are tabulated, and proarrhythmic effects and management strategies are discussed and pictorially illustrated.

Neuropsychiatric disorders in patients with heart failure: not to be ignored.

Among various neuropsychiatric disorders, depression and anxiety are commonly encountered in patients with heart failure (HF), reported in ≥ 50% of patients attending a HF clinic, but may frequently elude clinician's attention. Both disorders are associated with the development and progression of HF, incurring higher rates of morbidity/mortality, probably via physiologic and behavioral mechanisms. Patients with devices and/or advanced HF are more severely affected, especially early following device receipt. In addition, various other neuropsychiatric and neuropsychological disorders and symptoms of these and other disorders occur in and impact HF patients, including sleep disorders and cognitive impairment, which further interact with and amplify depression and anxiety. Mechanisms involved in the link between neuropsychiatric/neuropsychological disorders and HF may relate to pathophysiological processes, lifestyle factors, and behavioral patterns. Among the pathophysiological factors, inflammation, autonomic dysfunction, endothelial dysfunction, thrombotic mechanisms, and dysregulation of the hypothalamic-pituitary-adrenal axis may play a significant role as they are implicated in the pathogenesis, progression, and prognosis of HF. Multimodal psychiatric management strategies with flexible approaches, using antidepressants/anxiolytics/atypical antipsychotics and various psychotherapies such as cognitive behavioral therapy combined with exercise adjusted to patients' care and needs, appear promising in this patient group. Choosing agents with a higher efficacy/safety profile is a prudent strategy. Although depression and anxiety are risk factors for mortality in HF patients, indiscriminate use of psychiatric medications may not improve or even worsen survival when one neglects to closely monitor for potential proarrhythmic and other side effects. Newer meta-analytic data in HF patients indicate no increase in mortality for newer antidepressants, while secondary analyses show improved survival in patients who achieved remission of depressive symptoms.

Diet and Sudden Death: How to Reduce the Risk.

In addition to the association of dietary patterns, specific foods and nutrients with several diseases, including cardiovascular disease and mortality, there is also strong emerging evidence of an association of dietary patterns with the risk of sudden cardiac death (SCD). In this comprehensive review, data are presented and analyzed about foods and diets that mitigate the risk of ventricular arrhythmias (VAs) and SCD, but also about arrhythmogenic nutritional elements and patterns that seem to enhance or facilitate potentially malignant VAs and SCD. The antiarrhythmic or protective group comprises fish, nuts and other foods enriched in omega-3 polyunsaturated fatty acids, the Mediterranean and other healthy diets, vitamins E, A and D and certain minerals (magnesium, potassium, selenium). The arrhythmogenic-food group includes saturated fat, trans fats, ketogenic and liquid protein diets, the Southern and other unhealthy diets, energy drinks and excessive caffeine intake, as well as heavy alcohol drinking. Relevant antiarrhythmic mechanisms include modification of cell membrane structure by n-3 polyunsaturated fatty acids, their direct effect on calcium channels and cardiomyocytes and their important role in eicosanoid metabolism, enhancing myocyte electric stability, reducing vulnerability to VAs, lowering heart rate, and improving heart rate variability, each of which is a risk factor for SCD. Contrarily, saturated fat causes calcium handling abnormalities and calcium overload in cardiomyocytes, while a high-fat diet causes mitochondrial dysfunction that dysregulates a variety of ion channels promoting VAs and SCD. Free fatty acids have been considered proarrhythmic and implicated in facilitating SCD; thus, diets increasing free fatty acids, e.g., ketogenic diets, should be discouraged and replaced with diets enriched with polyunsaturated fatty acids, which can also reduce free fatty acids. All available relevant data on this important topic are herein reviewed, large studies and meta-analyses and pertinent advisories are tabulated, while protective (antiarrhythmic) and arrhythmogenic specific diet constituents are pictorially illustrated.

Low serum albumin: A neglected predictor in patients with cardiovascular disease.

Albumin, the most abundant circulating protein in blood, is an essential protein which binds and transports various drugs and substances, maintains the oncotic pressure of blood and influences the physiological function of the circulatory system. Albumin also has anti-inflammatory, antioxidant, and antithrombotic properties. Evidence supports albumin's role as a strong predictor of cardiovascular (CV) risk in several patient groups. Its protective role extends to those with coronary artery disease, heart failure, hypertension, atrial fibrillation, peripheral artery disease or ischemic stroke, as well as those undergoing revascularization procedures or with aortic stenosis undergoing transcatheter aortic valve replacement, and patients with congenital heart disease and/or endocarditis. Hypoalbuminemia is a strong prognosticator of increased all-cause and CV mortality according to several cohort studies and meta-analyses in hospitalized and non-hospitalized patients with or without comorbidities. Normalization of albumin levels before discharge lowers mortality risk, compared with hypoalbuminemia before discharge. Modified forms of albumin, such as ischemia modified albumin, also has prognostic value in patients with coronary or peripheral artery disease. When albumin is combined with other risk factors, such as uric acid or C-reactive protein, the prognostic value is enhanced. Although albumin supplementation may be a plausible approach, its efficacy has not been established and in patients with hypoalbuminemia, priority is focused on diagnosing and managing the underlying condition. The CV effects of hypoalbuminemia and relevant issues are considered in this review. Large cohort studies and meta-analyses are tabulated and the physiologic effects of albumin and the deleterious effects of low albumin are pictorially illustrated.

Atrial fibrillation-induced tachycardiomyopathy and heart failure: an underappreciated and elusive condition.

Many patients with persistent, chronic, or frequently recurring paroxysmal atrial fibrillation (AF) may develop a tachycardiomyopathy (TCM) with left ventricular (LV) dysfunction and heart failure (HF), which is reversible upon restoration and maintenance of sinus rhythm, when feasible, or via better and tighter ventricular rate (VR) control. Mechanisms involved in producing this leading cause of TCM (AF-TCM) include loss of atrial contraction, irregular heart rate, fast VR, neurohumoral activation, and structural myocardial changes. The most important of all mechanisms relates to optimal VR control, which seems to be an elusive target. Uncontrolled AF may also worsen preexisting LV dysfunction and exacerbate HF symptoms. Data, albeit less robust, also point to deleterious effects of slow VRs on LV function. Thus, a J-shaped relationship between VR and clinical outcome has been suggested, with the optimal VR control hovering at ~ 65 bpm, ranging between 60 and 80 bpm; VRs above and below this range may confer higher morbidity and mortality rates. A convergence of recent guidelines is noted towards a stricter rather than a more lenient VR control with target heart rate < 80 bpm at rest and < 110 bpm during moderate exercise which seems to prevent TCM or improve LV function and exercise capacity and relieve TCM-related symptoms and signs. Of course, restoring and maintaining sinus rhythm is always a most desirable target, when feasible, either with drugs or more likely with ablation. All these issues are herein reviewed, current guidelines are discussed and relevant data are tabulated and pictorially illustrated.

Gut Microbiota and Cardiovascular Disease: Symbiosis Versus Dysbiosis.

The gut microbiome interacts with host physiology through various mechanisms, including the cardiovascular (CV) system. A healthy microbiome has the ability to process and digest complex carbohydrates into short-chain fatty acids (SCFA). These SCFA function as signaling molecules, immune-modulating molecules, and energy sources. However, when the microbiome is altered, it produces gut dysbiosis with overgrowth of certain bacteria that may lead to overproduction of trimethylamine-N-oxide (TMAO) from the metabolism of phosphatidylcholine, choline, and carnitine; dysbiosis also leads to increased intestinal permeability allowing the microbiome-derived lipopolysaccharide (LPS), a bacterial endotoxin, to enter the blood circulation, triggering inflammatory responses. An altered gastrointestinal (GI) tract environment and microbiome- derived metabolites are associated with CV events. Disrupted content and function of the microbiome leading to elevated TMAO and LPS levels, altered bile acid metabolism pathways, and SCFA production are associated with an increased risk of CV diseases (CVD), including atherosclerosis, myocardial infarction, thrombosis, arrhythmias, and stroke. Therapeutic interventions that may favorably influence a dysbiotic GI tract profile and promote a healthy microbiome may benefit the CV system and lead to a reduction of CVD incidence in certain situations. These issues are herein reviewed with a focus on the spectrum of microbiota-related CVD, the mechanisms involved, and the potential use of microbiome modification as a possible therapeutic intervention.

The proarrhythmic conundrum of alcohol intake.

The arrhythmogenic potential of alcohol consumption that leads to cardiac arrhythmia development includes the induction of both atrial and ventricular arrhythmias, with atrial fibrillation (AF) being the commonest alcohol-related arrhythmia, even with low/moderate alcohol consumption. Arrhythmias occur both with acute and chronic alcohol use. The "Holiday Heart Syndrome" relates to the occurrence of AF, most commonly following weekend or public holiday binge drinking; however, other arrhythmias may also occur, including other supraventricular arrhythmias, and occasionally even frequent ventricular premature beats and a rare occurrence of ventricular tachycardia. Arrhythmias in individuals with alcohol use disorder, in addition to AF, may comprise ventricular arrhythmias (VAs) that may be potentially fatal leading to cardiac arrest. The effects of alcohol on triggering VAs appear to be dose-dependent, observed more commonly in heavy drinkers, both in healthy individuals and patients with underlying structural heart disease, including ischemic heart disease and alcoholic cardiomyopathy. Men appear to be affected at higher dosages of alcohol, while women can suffer from arrhythmias at lower dosages. On the other hand, low to moderate consumption of alcohol may confer some protection from serious VAs and cardiac arrest (J- or U-curve phenomenon); however, abstinence is the optimal strategy. These issues as they relate to alcohol-induced proarrhythmia are herein reviewed, with the large studies and meta-analyses tabulated and the arrhythmogenic mechanisms pictorially illustrated.

Update on Cilostazol: A Critical Review of Its Antithrombotic and Cardiovascular Actions and Its Clinical Applications.

Cilostazol, a phosphodiesterase III inhibitor, has vasodilating and antiplatelet properties with a low rate of bleeding complications. It has been used over the past 25 years for improving intermittent claudication in patients with peripheral artery disease (PAD). Cilostazol also has demonstrated efficacy in patients undergoing percutaneous revascularization procedures for both PAD and coronary artery disease. In addition to its antithrombotic and vasodilating actions, cilostazol also inhibits vascular smooth muscle cell proliferation via phosphodiesterase III inhibition, thus mitigating restenosis. Accumulated evidence has shown that cilostazol, due to its "pleiotropic" effects, is a useful, albeit underutilized, agent for both coronary artery disease and PAD. It is also potentially useful after ischemic stroke and is an alternative in those who are allergic or intolerant to classical antithrombotic agents (eg, aspirin or clopidogrel). These issues are herein reviewed together with the pharmacology and pharmacodynamics of cilostazol. Large studies and meta-analyses are presented and evaluated. Current guidelines are also discussed, and the spectrum of cilostazol's actions and therapeutic applications are illustrated.

The Cardiovascular Benefits of Caffeinated Beverages: Real or Surreal? "Metron Ariston - All in Moderation".

Caffeinated beverages are the most widely consumed beverages globally with coffee and tea as the two most prominent sources of caffeine. Caffeine content varies across different types of beverages. In addition to caffeine, coffee and tea have other biologically active compounds, and all may affect general and cardiovascular (CV) health. Moderate caffeine consumption (<300-400 mg/day), regardless of the source, is considered safe by both European and US Health Authorities, as it is not associated with adverse health and CV effects, while it may confer certain health benefits. There is a nonlinear association between coffee ingestion and CV risk; moderate coffee drinking is inversely significantly associated with CV risk, with the highest benefit at 2-4 cups per day, while heavy coffee drinking might confer increased risk. With regards to tea, due to a lower caffeine content per serving, its consumption is only limited by the total caffeine daily intake. Both these caffeinated beverages, coffee and tea, have additional phenolic compounds, with anti-oxidant and anti-inflammatory activities, which confer cardioprotective benefits. Of the several coffee compounds, chloroacetic acids and melanoidins offer such beneficial effects, while diterpenes may have unfavorable effects on lipids. Most of the tea ingredients (polyphenols) are cardioprotective. A major concern relates to energy drinks with their much higher caffeine content which puts individuals, especially adolescents and young adults, at high health and CV risk. All these issues are herein discussed, including pertinent studies and meta-analyses, pathogenetic mechanisms involved and relevant recommendations from health authorities.

Lipoprotein(a) and Cardiovascular Disease: A Missing Link for Premature Atherosclerotic Heart Disease and/or Residual Risk.

ABSTRACT: Lipoprotein(a) or lipoprotein "little a" [Lp(a)] is an under-recognized causal risk factor for cardiovascular (CV) disease (CVD), including coronary atherosclerosis, aortic valvular stenosis, ischemic stroke, heart failure, and peripheral arterial disease. Elevated plasma Lp(a) (≥50 mg/dL or ≥100 nmol/L) is commonly encountered in almost 1 in 5 individuals and confers a higher CV risk compared with those with normal Lp(a) levels, although such normal levels have not been generally agreed upon. Elevated Lp(a) is considered a cause of premature and accelerated atherosclerotic CVD. Thus, in patients with a positive family or personal history of premature coronary artery disease (CAD), Lp(a) should be measured. However, elevated Lp(a) may confer increased risk for incident CAD even in the absence of a family history of CAD, and even in those who have guideline-lowered LDL cholesterol (<70 mg/dL) and continue to have a persisting CV residual risk. Thus, measurement of Lp(a) will have a significant clinical impact on the assessment of atherosclerotic CVD risk, and will assume a more important role in managing patients with CVD with the advent and clinical application of specific Lp(a)-lowering therapies. Conventional therapeutic approaches like lifestyle modification and statin therapy remain ineffective at lowering Lp(a). Newer treatment modalities, such as gene silencing via RNA interference with use of antisense oligonucleotide(s) or small interfering RNA molecules targeting Lp(a), seem very promising. These issues are herein reviewed, accumulated data are scrutinized, meta-analyses and current guidelines are tabulated, and Lp(a)-related CVDs and newer therapeutic modalities are pictorially illustrated.

COVID-19 infection and body weight: A deleterious liaison in a J-curve relationship.

During the course of the COVID-19 pandemic, obesity has been shown to be an independent risk factor for high morbidity and mortality. Obesity confers poor outcomes in younger (<60 years) patients, an age-group considered low-risk for complications, a privilege that is negated by obesity. Findings are consistent, the higher the body mass index (BMI) the worse the outcomes. Ectopic (visceral) obesity also promotes proinflammatory, prothrombotic, and vasoconstrictive states, thus enhancing the deleterious effects of COVID-19 disease. Less, albeit robust, evidence also exists for a higher risk of COVID-19 infection incurred with underweight. Thus, the relationship of COVID-19 and BMI has a J-curve pattern, where patients with both overweight/obesity and underweight are more susceptible to the ailments of COVID-19. The pathophysiology underlying this link is multifactorial, mostly relating to the inflammatory state characterizing obesity, the impaired immune response to infectious agents coupled with increased viral load, the overexpression in adipose tissue of the receptors and proteases for viral entry, an increased sympathetic activity, limited cardiorespiratory reserve, a prothrombotic milieu, and the associated comorbidities. All these issues are herein reviewed, the results of large studies and meta-analyses are tabulated and the pathogenetic mechanisms and the BMI relationship with COVID-19 are pictorially illustrated.

Electrocardiography of cardiac resynchronization therapy: Pitfalls and practical tips.

Cardiac resynchronization therapy (CRT) has been established as an effective mode of therapy in patients with heart failure and concurrent cardiac dyssynchrony, principally in the form of left bundle branch block (LBBB). The widespread use of CRT has ushered in a new landscape in 12-lead electrocardiography (ECG). ECG readings in these patients are most important to guide troubleshooting and also appropriate device programming, as well as discerning and managing nonresponders. A set of four ECG recordings need to accompany each patient with a CRT device, including a baseline ECG and recordings from monochamber (right and left ventricular) and biventricular pacing, which can be compared against a new recording to facilitate the evaluation of proper versus problematic biventricular pacing. Precordial ECG leads V1/2 acquired at the fourth intercostal space and limb leads, I and III, together with a quick assessment of perpendicular leads I and aVF to determine the quadrant of the QRS axis in the hexaxial diagram, may provide the framework for proper ECG interpretation in these patients. This important issue of 12-lead ECG in CRT patients is herein reviewed, pitfalls are pointed out and practical tips are provided for ECG reading to help recognize and manage problems with CRT device function. Furthermore, several pertinent ECG recordings and tabulated data are provided, and an algorithm is suggested that integrates prior algorithms and relevant information from current literature.

COVID-19 Infection: A Neuropsychiatric Perspective.

As a potentially life-threatening disease with no definitive treatment and without fully implemented population-wide vaccination, COVID-19 has created unprecedented turmoil in socioeconomic life worldwide. In addition to physical signs from the respiratory and many other systems, the SARS-CoV-2 virus produces a broad range of neurological and neuropsychiatric problems, including olfactory and gustatory impairments, encephalopathy and delirium, stroke and neuromuscular complications, stress reactions, and psychoses. Moreover, the psychosocial impact of the pandemic and its indirect effects on neuropsychiatric health in noninfected individuals in the general public and among health care workers are similarly far-ranging. In addition to acute neuropsychiatric manifestations, COVID-19 may also produce late neuropsychiatric sequelae as a function of the psychoneuroimmunological cascade that it provokes. The present article presents a state-of-the-science review of these issues through an integrative review and synthesis of case series, large-cohort studies, and relevant meta-analyses. Heuristics for evaluation and further study of the neuropsychiatric manifestations of SARS-CoV-2 infection are offered.

COVID-19 and Acute Myocardial Injury and Infarction: Related Mechanisms and Emerging Challenges.

In the era of the coronavirus disease 2019 (COVID-19) pandemic, acute cardiac injury (ACI), as reflected by elevated cardiac troponin above the 99th percentile, has been observed in 8%-62% of patients with COVID-19 infection with highest incidence and mortality recorded in patients with severe infection. Apart from the clinically and electrocardiographically discernible causes of ACI, such as acute myocardial infarction (MI), other cardiac causes need to be considered such as myocarditis, Takotsubo syndrome, and direct injury from COVID-19, together with noncardiac conditions, such as pulmonary embolism, critical illness, and sepsis. Acute coronary syndromes (ACS) with normal or near-normal coronary arteries (ACS-NNOCA) appear to have a higher prevalence in both COVID-19 positive and negative patients in the pandemic compared to the pre-pandemic era. Echocardiography, coronary angiography, chest computed tomography and/or cardiac magnetic resonance imaging may render a correct diagnosis, obviating the need for endomyocardial biopsy. Importantly, a significant delay has been recorded in patients with ACS seeking advice for their symptoms, while their routine care has been sharply disrupted with fewer urgent coronary angiographies and/or primary percutaneous coronary interventions performed in the case of ST-elevation MI (STEMI) with an inappropriate shift toward thrombolysis, all contributing to a higher complication rate in these patients. Thus, new challenges have emerged in rendering a diagnosis and delivering treatment in patients with ACI/ACS in the pandemic era. These issues, the various mechanisms involved in the development of ACI/ACS, and relevant current guidelines are herein reviewed.

Cardiovascular implications and complications of the coronavirus disease-2019 pandemic: a world upside down.

PURPOSE OF REVIEW: The new pandemic of coronavirus disease-2019 (COVID-19) has produced a global tumult and has overburdened national health systems. We herein discuss the cardiovascular implications and complications of this pandemic analyzing the most recent data clustered over the last several months. RECENT FINDINGS: COVID-19 afflicts the cardiovascular system producing acute cardiac injury in 10-20% of cases with mild disease but in greater than 50-60% in severe cases, contributing to patients' demise. Other cardiovascular complications include arrhythmias, heart failure, pulmonary embolism and shock. Off-label therapies are being trialed with their own inherent cardiovascular risks, while supportive therapies currently dominate, until more specific and effective antiviral therapies and vaccinations become available. A controversial issue relates to the safety of drugs blocking the renin--angiotensin system as an angiotensin-converting enzyme (ACE) homologue, ACE2, serves as the receptor for viral entry into host cells. However, to-date, no harm has been proven for these drugs. SUMMARY: In the cardiovascular system, COVID-19 can induce acute cardiac injury, arrhythmias, heart failure, pulmonary embolism, shock and death, whereas anti-COVID therapies also confer serious cardiovascular side-effects. Ongoing extensive efforts focus on specific vaccines and antivirals. Meanwhile, cardiovascular risk factors and diseases should be jointly controlled according to current evidence-based guidelines.