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Dissemination of scientific content has been amplified with increasing use of social media (SoMe) in cardiovascular (CV) medicine ([1][1]). Traditionally, the performance of a scholarly journal paper is measured by the number of times it is cited. A newer metric, the Altmetric Attention Score (AAS

There is a growing interest concerning MINOCA in the clinical practice. The aim of this study is to analyze the clinical profile and prognosis of MINOCA patients compared to those with myocardial infarction with obstructive lesions. Analytical and observational study developed in a University

The term early repolarization has been in use for more than 50 years. This electrocardiographic pattern was considered benign until 2008, when it was linked to sudden cardiac arrest due to idiopathic ventricular fibrillation. Much confusion over the definition of early repolarization followed. Thus, the objective of this paper was to prepare an agreed definition to facilitate future research in this area. The different definitions of the early repolarization pattern were reviewed to delineate the electrocardiographic measures to be used when defining this pattern. An agreed definition has been established, which requires the peak of an end-QRS notch and/or the onset of an end-QRS slur as a measure, denoted Jp, to be determined when an interpretation of early repolarization is being considered. One condition for early repolarization to be present is Jp >= 0.1 mV, while ST-segment elevation is not a required criterion.

The term early repolarization has been in use for more than 50 years. This electrocardiographic pattern was considered benign until 2008, when it was linked to sudden cardiac arrest due to idiopathic ventricular fibrillation. Much confusion over the definition of early repolarization followed. Thus, the objective of this paper was to prepare an agreed definition to facilitate future research in this area. The different definitions of the early repolarization pattern were reviewed to delineate the electrocardiographic measures to be used when defining this pattern. An agreed definition has been established, which requires the peak of an end-QRS notch and/or the onset of an end-QRS slur as a measure, denoted Jp, to be determined when an interpretation of early repolarization is being considered. One condition for early repolarization to be present is Jp ≥0.1 mV, while ST-segment elevation is not a required criterion.

Item does not contain fulltext Until recently, vitamin K antagonists were the only available oral anticoagulants, but with numerous limitations that prompted the introduction of new oral anticoagulants targeting the single coagulation enzymes thrombin (dabigatran) or factor Xa (apixaban, rivaroxaban, and edoxaban) and given in fixed doses without coagulation monitoring. Here we review the pharmacology and the results of clinical trials with these new agents in stroke prevention in atrial fibrillation and secondary prevention after acute coronary syndromes, providing perspectives on their future incorporation into clinical practice. In phase III trials in atrial fibrillation, compared with warfarin, dabigatran etexilate 150 mg B.I.D. reduced the rates of stroke/systemic embolism without any difference in major bleeding; dabigatran etexilate 110 mg B.I.D. had similar efficacy with decreased bleeding; apixaban 5 mg B.I.D. reduced stroke, systemic embolism, and mortality as well as major bleeding; and rivaroxaban 20 mg Q.D. was noninferior to warfarin for stroke and systemic embolism without a difference in major bleeding. All these agents reduced intracranial hemorrhage. Edoxaban is currently being evaluated in a further large phase III trial. Apixaban and rivaroxaban were evaluated in phase III trials for prevention of recurrent ischemia in patients with acute coronary syndromes who were mostly receiving dual antiplatelet therapy, with conflicting results on efficacy but consistent results for increased major bleeding. Overall, the new oral anticoagulants are poised to replace vitamin K antagonists for many patients with atrial fibrillation and may have a role after acute coronary syndromes. Although convenient to administer and manage, they present challenges that need to be addressed.

Objectives. The purpose of the present study was to examine the expression of the endothelial-type nitric oxide synthase (NOS III) and the inducible-type NOS (NOS II) in human myocardium and their regulation in heart failure from patients with different etiologies. Background. In heart failure, plasma levels of nitrates were found to be elevated. However, data on myocardial NOS expression in heart failure are conflicting. Methods. Using RNase protection analysis and Western blotting, the expression of NOS III and NOS II was investigated in ventricular myocardium from nonfailing (NF) hearts (n = 5) and from failing hearts of patients with idiopathic dilated cardiomyopathy (dCMP, n = 14), ischemic cardiomyopathy (iCMP, n = 9) or postmyocarditis cardiomyopathy (mCMP, n = 7). Furthermore, immunohistochemical studies were performed to localize NOS III and NOS II within the ventricular myocardium. Results. In failing human hearts, NOS III mRNA levels were increased to 180% in dCMP, 200% in iCMP and to 210% in mCMP as compared to NF hearts. Similarly, in Western blots (using constitutively expressed beta-tubulin as a reference) NOS III protein expression was increased about twofold in failing compared to NF hearts. Immunohistochemical studies with a selective antibody to NOS III showed no obvious differences in the staining of the endothelium of cardiac blood vessels from NF and failing human hearts. However, NOS III-immunoreactivity in cardiomyocytes was significantly more intense in failing compared to NF hearts. Low expression of NOS II mRNA was detected in only 2 of 30 failing human hearts and was not found in NF hearts. Inducible-type NOS protein was undetectable in either group. Conclusions. We conclude that the increased NOS III expression in the ventricular myocardium of failing human hearts may contribute to the contractile dysfunction observed in heart failure and/or may play a role in morphologic alterations such as hypertrophy and apoptosis of cardiomyocytes.

Although the use of oral anticoagulants (vitamin K antagonists) has been abandoned in primary cardiovascular prevention due to lack of a favorable benefit-to-risk ratio, the indications for aspirin use in this setting continue to be a source of major debate, with major international guidelines providing conflicting recommendations. Here, we review the evidence in favor and against aspirin therapy in primary prevention based on the evidence accumulated so far, including recent data linking aspirin with cancer protection. While awaiting the results of several ongoing studies, we argue for a pragmatic approach to using low-dose aspirin in primary cardiovascular prevention and suggest its use in patients at high cardiovascular risk, defined as ≥2 major cardiovascular events (death, myocardial infarction, or stroke) projected per 100 person-years, who are not at increased risk of bleeding.

Until recently, vitamin K antagonists were the only available oral anticoagulants, but with numerous limitations that prompted the introduction of new oral anticoagulants targeting the single coagulation enzymes thrombin (dabigatran) or factor Xa (apixaban, rivaroxaban, and edoxaban) and given in fixed doses without coagulation monitoring. Here we review the pharmacology and the results of clinical trials with these new agents in stroke prevention in atrial fibrillation and secondary prevention after acute coronary syndromes, providing perspectives on their future incorporation into clinical practice. In phase III trials in atrial fibrillation, compared with warfarin, dabigatran etexilate 150 mg B.I.D. reduced the rates of stroke/systemic embolism without any difference in major bleeding; dabigatran etexilate 110 mg B.I.D. had similar efficacy with decreased bleeding; apixaban 5 mg B.I.D. reduced stroke, systemic embolism, and mortality as well as major bleeding; and rivaroxaban 20 mg Q.D. was noninferior to warfarin for stroke and systemic embolism without a difference in major bleeding. All these agents reduced intracranial hemorrhage. Edoxaban is currently being evaluated in a further large phase III trial. Apixaban and rivaroxaban were evaluated in phase III trials for prevention of recurrent ischemia in patients with acute coronary syndromes who were mostly receiving dual antiplatelet therapy, with conflicting results on efficacy but consistent results for increased major bleeding. Overall, the new oral anticoagulants are poised to replace vitamin K antagonists for many patients with atrial fibrillation and may have a role after acute coronary syndromes. Although convenient to administer and manage, they present challenges that need to be addressed.

QT dispersion from the 12 lead ECG has been extensively evaluated as a risk parameter in pts prone to arrhythmias. Usually, this parameter is assessed directly from the ECG tracing by means of a magnifying glass and a digitizing pad with reproducibility and accuracy not being optimal. We therefore developed a software program with a graphical interface permitting conversion of a scanned image of the ECG on paper to a digital ECG function (sampling rate 500 or 1000 Hz) which can then be analyzed by a second interactive computer program for standard ECG intervals, QT dispersion and other repolarization parameters (JTpeak, T areas, T peak to T end interval). Digitally available ECGs can also be converted to a format analyzable by the program. The respective signals are processed channel-by-channel with enlarged high resolution display on a 20″ computer screen. The computer program uses customized algorithms to detect important features of the ECG waveforms (Q onset, J point, T peak, and T end for ECG signals) and then displays colored vertical spikes superimposed on the signal marking these points with high resolution for confirmation or manual correction by the observer. The processed data are automatically written to a spreadsheet for further processing. With this methodology accuracy and reproducibility of QT intervals and ECG parameters of dispersion of repolarization can be increased and parameters not easily measurable on paper can be determined (T wave areas).

Cardiac remodeling is generally accepted as a determinant of the clinical course of heart failure (HF). Defined as genome expression resulting in molecular, cellular and interstitial changes and manifested clinically as changes in size, shape and function of the heart resulting from cardiac load or injury, cardiac remodeling is influenced by hemodynamic load, neurohormonal activation and other factors still under investigation. Although patients with major remodeling demonstrate progressive worsening of cardiac function, slowing or reversing remodeling has only recently become a goal of HF therapy. Mechanisms other than remodeling can also influence the course of heart disease, and disease progression may occur in other ways in the absence of cardiac remodeling. Left ventricular end-diastolic and end-systolic volume and ejection fraction data provide support for the beneficial effects of therapeutic agents such as angiotensin-converting enzyme (ACE) inhibitors and beta-adrenergic blocking agents on the remodeling process. These agents also provide benefits in terms of morbidity and mortality. Although measurement of ejection fraction can reliably guide initiation of treatment in HF, opinions differ regarding the value of ejection fraction data in guiding ongoing therapy. The role of echocardiography or radionuclide imaging in the management and monitoring of HF is as yet unclear. To fully appreciate the potential benefits of HF therapies, clinicians should understand the relationship between remodeling and HF progression. Their patients may then, in turn, acquire an improved understanding of their disease and the treatments they are given.