Clinical implications of combination proton pump inhibitor and triple therapies in patients with atrial fibrillation following percutaneous intervention: a guide for clinicians.

INTRODUCTION: Patients on systemic oral anticoagulation with vitamin K antagonists (VKA) or non-vitamin K oral anticoagulants (NOAC) often require triple therapy following percutaneous coronary intervention, substantially increasing the risk of bleeding. Gastroprotective agents like proton pump inhibitors (PPI) are often employed to mitigate this risk, despite potential competitive inhibition between P2Y12-receptor inhibitors, NOACs, and VKAs. While the interactions and clinical outcomes of PPIs and DAPT have been frequently explored in literature, not many studies have evaluated the same outcomes for triple therapy. AREAS COVERED: This comprehensive narrative review of three studies on PPIs and triple from the PubMed/MEDLINE database supplemented by 23 other relevant studies aims to use the available literature to analyze the potential interactions between PPIs and triple therapy while shedding light on their mechanisms, clinical implications, and areas for optimization. EXPERT OPINION: If triple therapy is indicated following PCI, then patients at high-risk for bleeding may benefit from transition to apixaban and a PPI to lower the risk of gastrointestinal bleeding. More research is needed to determine the role of PPIs in triple therapies in prevention of gastrointestinal bleeding or potentiation of other adverse outcomes.

Anterior ST elevation in a patient with RBBB.

A 79-year-old male with a history of coronary artery disease presented to the Emergency Department with chest pain. ECG showed RBBB with mild ST elevation and positive T waves in I, aVL and V2. In patients with RBBB lack of ST depression and T wave inversion in the anterior leads could signify ischemia secondary to left anterior descending coronary artery occlusion. However, the patient did not have acute coronary syndrome and the presenting ECG was comparable to an ECG recorded five years earlier.

Pharmacotherapy for Coronary Artery Disease and Acute Coronary Syndrome in the Aging Population.

PURPOSE OF REVIEW: To provide a comprehensive summary of relevant studies and evidence concerning the utilization of different pharmacotherapeutic and revascularization strategies in managing coronary artery disease and acute coronary syndrome specifically in the older adult population. RECENT FINDINGS: Approximately 30% to 40% of hospitalized patients with acute coronary syndrome are older adults, among whom the majority of cardiovascular-related deaths occur. When compared to younger patients, these individuals generally experience inferior clinical outcomes. Most clinical trials assessing the efficacy and safety of various therapeutics have primarily enrolled patients under the age of 75, in addition to excluding those with geriatric complexities. In this review, we emphasize the need for a personalized and comprehensive approach to pharmacotherapy for coronary heart disease and acute coronary syndrome in older adults, considering concomitant geriatric syndromes and age-related factors to optimize treatment outcomes while minimizing potential risks and complications. In the realm of clinical practice, cardiovascular and geriatric risks are closely intertwined, with both being significant factors in determining treatments aimed at reducing negative outcomes and attaining health conditions most valued by older adults.

Electronic ventricular pacing at the end of the QRS complex: Is it abnormal?

An 82-year-old man with ischemic cardiomyopathy, heart failure with reduced ejection fraction and Medtronic biventricular ICD presented with shortness of breath. His ECG is presented with shortness of breath. ECG shows atrial sensed, electronic ventricular pacing. At the end of each QRS complex there is another pacemaker stimulus. This represents typical case of cardiac contractility modulation therapy and not pacemaker malfunction.

Why do we keep missing left circumflex artery myocardial infarctions?

BACKGROUND: Diagnosis of left circumflex artery (LCx) myocardial infarctions via 12­lead electrocardiogram (ECG) has posed a challenge to healthcare professionals for many years. METHODS AND RESULTS: A retrospective observational study was performed to analyze patients admitted with myocardial infarction. The study used electronic medical records and specific ICD-10 codes to identify eligible patients, resulting in 2032 encounters. After independent adjudication of cardiac biomarkers, coronary angiography, and electrocardiographic changes, a final patient population of 58 encounters with acute occlusion myocardial infarction (OMI) with a culprit LCx lesion was established. OMI was defined as a lesion with either thrombolysis in myocardial infarction flow (TIMI) 0-2 or TIMI 3 with Troponin I > 1 ng/mL (Reference range 0.00-0.03 ng/mL). ECGs of these patients were then independently evaluated and grouped into 8 different classifications based on the presence or absence of ST elevation and/or depression in corresponding leads. ECG patterns and anatomical characteristics (proximal or distal to the first obtuse marginal artery) of the LCx lesions were then correlated. The appropriateness of triage and delay in reperfusion therapy were also assessed. Those with a left dominant or codominant circulation, and with LCx lesions proximal to the first obtuse marginal artery, were more likely to present with no or subtle ST-segment changes that led to delays in reperfusion therapy. CONCLUSIONS: Patients with left or codominant coronary artery circulation, with OMI proximal to the first obtuse marginal artery, may be less likely to have "classic" findings of ST-segment elevation on ECG due to cancellation forces in the limb leads.

Do We Still Need Aspirin in Coronary Artery Disease?

Aspirin has for some time been used as a first-line treatment for acute coronary syndromes, including ST-elevation myocardial infarction, for secondary prevention of established coronary disease, and for primary prevention in patients at risk of coronary artery disease. Although aspirin has been in use for decades, the available evidence for its efficacy largely predates the introduction of other drugs, such as statins and P2Y12 inhibitors. Based on recent trials, the recommendation for aspirin use as primary prevention has been downgraded. In addition, P2Y12 inhibitors given as a single antiplatelet therapy have been associated with a lower incidence of bleeding than dual antiplatelet therapy in combination with aspirin in patients with stable and unstable coronary artery disease. The aim of this review is to discuss the role of aspirin considering the available evidence for primary prevention, secondary prevention for stable coronary artery disease or acute coronary syndromes, and after percutaneous coronary intervention or coronary artery bypass revascularization.

Effects of Dapagliflozin on Myocardial Gene Expression in BTBR Mice with Type 2 Diabetes.

BACKGROUND: Dapagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, is approved for the treatment of type 2 diabetes, heart failure, and chronic kidney disease. DAPA-HF and DELIVER trial results demonstrate that the cardiovascular protective effect of dapagliflozin extends to non-diabetic patients. Hence, the mechanism-of-action may extend beyond glucose-lowering and is not completely elucidated. We have previously shown that dapagliflozin reduces cardiac hypertrophy, inflammation, fibrosis, and apoptosis and increases ejection fraction in BTBR mice with type 2 diabetes. METHODS: We conducted a follow-up RNA-sequencing study on the heart tissue of these animals and performed differential expression and Ingenuity Pathway analysis. Selected markers were confirmed by RT-PCR and Western blot. RESULTS: SGLT2 had negligible expression in heart tissue. Dapagliflozin improved cardiac metabolism by decreasing glycolysis and pyruvate utilization enzymes, induced antioxidant enzymes, and decreased expression of hypoxia markers. Expression of inflammation, apoptosis, and hypertrophy pathways was decreased. These observations corresponded to the effects of dapagliflozin in the clinical trials.

Left septal fascicular block: Evidence, causes, and diagnostic criteria.

The existence of a tetrafascicular intraventricular conduction system is widely accepted by researchers. In this review, we have updated the criteria for left septal fascicular block (LSFB) and the differential diagnosis of prominent anterior QRS forces. More and more evidence points to the fact that the main cause of LSFB is critical proximal stenosis of the left anterior descending coronary artery before its first septal perforator branch. The most important characteristic of LSFB that has been incorporated in the corresponding diagnostic electrocardiographic criteria is its transient/intermittent nature mostly observed in clinical scenarios of acute (ie, acute coronary syndrome including vasospastic angina) or chronic (ie, exercise-induced ischemia) ischemic coronary artery disease. In addition, the phenomenon proved to be phase 4 bradycardia rate dependent and induced by early atrial extrastimulus. Finally, we believe that intermittent LSFB has the same clinical significance as "Wellens syndrome" and the "de Winter pattern" in the acute coronary syndrome scenario.

Dual Antiplatelet Therapy: A Concise Review for Clinicians.

Dual antiplatelet therapy (DAPT) combines two antiplatelet agents to decrease the risk of thrombotic complications associated with atherosclerotic cardiovascular diseases. Emerging data about the duration of DAPT is being published continuously. New approaches are trying to balance the time, benefits, and risks for patients taking DAPT for established cardiovascular diseases. Short-term dual DAPT of 3-6 months, or even 1 month in high-bleeding risk patients, is equivalent in terms of efficacy and effectiveness compared to long-term DAPT for patients who experienced percutaneous coronary intervention in an acute coronary syndrome setting. Prolonged DAPT beyond 12 months reduces stent thrombosis, major adverse cardiovascular events, and myocardial infarction rates but increases bleeding risk. Extended DAPT does not significantly benefit stable coronary artery disease patients in reducing stroke, myocardial infarction, or cardiovascular death. Ticagrelor and aspirin reduce cardiovascular events in stable coronary artery disease with diabetes but carry a higher bleeding risk. Antiplatelet therapy duration in atrial fibrillation patients after percutaneous coronary intervention depends on individual characteristics and bleeding risk. Antiplatelet therapy is crucial for post-coronary artery bypass graft and transcatheter aortic valve implantation; Aspirin (ASA) monotherapy is preferred. Antiplatelet therapy duration in peripheral artery disease depends on the scenario. Adding vorapaxar and cilostazol may benefit secondary prevention and claudication, respectively. Carotid artery disease patients with transient ischemic attack or stroke benefit from antiplatelet therapy and combining ASA and clopidogrel is more effective than ASA alone. The optimal duration of DAPT after carotid artery stenting is uncertain. Resistance to ASA and clopidogrel poses an incremental risk of deleterious cardiovascular events and stroke. The selection and duration of antiplatelet therapy in patients with cardiovascular disease requires careful consideration of both efficacy and safety outcomes. The use of combination therapies may provide added benefits but should be weighed against the risk of bleeding. Further research and clinical trials are needed to optimize antiplatelet treatment in different patient populations and clinical scenarios.

Circular RNA as Therapeutic Targets in Atherosclerosis: Are We Running in Circles?

Much attention has been paid lately to harnessing the diagnostic and therapeutic potential of non-coding circular ribonucleic acids (circRNAs) and micro-RNAs (miRNAs) for the prevention and treatment of cardiovascular diseases. The genetic environment that contributes to atherosclerosis pathophysiology is immensely complex. Any potential therapeutic application of circRNAs must be assessed for risks, benefits, and off-target effects in both the short and long term. A search of the online PubMed database for publications related to circRNA and atherosclerosis from 2016 to 2022 was conducted. These studies were reviewed for their design, including methods for developing atherosclerosis and the effects of the corresponding atherosclerotic environment on circRNA expression. Investigated mechanisms were recorded, including associated miRNA, genes, and ultimate effects on cell mechanics, and inflammatory markers. The most investigated circRNAs were then further analyzed for redundant, disparate, and/or contradictory findings. Many disparate, opposing, and contradictory effects were observed across experiments. These include levels of the expression of a particular circRNA in atherosclerotic environments, attempted ascertainment of the in toto effects of circRNA or miRNA silencing on atherosclerosis progression, and off-target, cell-specific, and disease-specific effects. The high potential for detrimental and unpredictable off-target effects downstream of circRNA manipulation will likely render the practice of therapeutic targeting of circRNA or miRNA molecules not only complicated but perilous.

Interpreting the ECG in patients with chest pain and right bundle branch block: A case report.

A patient with right bundle branch block (RBBB) presented with chest pain. An ECG showed ST-elevation in leads V1, V2, and aVR, with widespread ST-depression in leads II, aVF, I, aVL, and V4-6. The initial ECG interpretation missed ST-elevation myocardial infarction (STEMI), as ST-elevation thresholds were not reached. Non-urgent angiography showed severe left anterior descending artery stenosis requiring percutaneous coronary intervention. The course was complicated by cardiac arrest necessitating resuscitation and dual chamber pacemaker placement with left bundle branch pacing. This case report outlines the deficiencies of the current voltage criteria for identification of anterior STEMI in patients with RBBB.