From a pathogenetic point of view, heart failure (HF) is characterized by the activation of several neurohumoral pathways with a role in maintaining the cardiac output and the adequate perfusion pressure in target organs and tissues. Decreased cardiac output in HF with reduced ejection fraction causes activation of the sympathetic nervous system, the renin angiotensin aldosterone system, arginine-vasopressin system, natriuretic peptides, and endothelin, all of which cause water and salt retention in the body. As a result, patients will present clinically as the main symptoms: dyspnea and peripheral edema caused by fluid redistribution to the lungs and/or by fluid overload. By studying these pathophysiological mechanisms, biomarkers with a prognostic and therapeutic role in the management of edema were identified in patients with HF with low ejection fraction. This review aims to summarize the current data from the specialty literature of such biomarkers with a role in the pathogenesis of edema in HF with low ejection fraction. These biomarkers may be the basis for risk stratification and the development of new therapeutic means in the treatment of edema in these patients.
The baseline electrocardiogram (ECG) is less informative in neurally mediated syncope (NMS) than in arrhythmic syncope. However, some of the ECG patterns present in NMS can have diagnostic and prognostic value in such patients. Electrocardiographic documentation of a syncopal spell and thus identification of the ECG changes can be performed during tilt table test (TTT) or during prolonged ECG monitoring. This work reviews the specific ECG patterns in NMS, which are primarily related to the cardioinhibitory reflex. In addition, there are other ECG findings present in patients with NMS that are being analyzed, such as increased heart rate variability as well as specific QRS voltage patterns. In addition to the diagnostic and prognostic value, these ECG patterns in NMS may help improving the selection of patients for pacemaker implant.
We present the case of a 71-year-old man with history of smoking, pulmonary emphysema, hypertension, multivessel coronary artery disease and prior coronary artery bypass graft surgery who presented with spontaneous right-sided pneumothorax associated with phasic changes of the QRS amplitude on the electrocardiogram. While several case reports have described QRS amplitude changes associated with left-sided pneumothorax, reports of phasic ECG changes in right-sided pneumothorax are exceedingly rare. Such changes, when present in a patient with sudden onset chest pain and dyspnea, should prompt a diagnostic workup for possible pneumothorax.
Among the different types, immunoglobulin light chain (AL) cardiac amyloidosis is associated with the highest morbidity and mortality. The outcome, however, is significantly better when an early diagnosis is made and treatment initiated promptly. We present a case of cardiac amyloidosis with left ventricular hypertrophy criteria on the electrocardiogram. After 9 months of follow-up, the patient developed low voltage in the limb leads, while still maintaining the Cornell criteria for left ventricular hypertrophy as well. The relative apical sparing by the disease process, as well as decreased cancellation of the opposing left ventricular walls could be responsible for this phenomenon. The discordance between the voltage in the frontal leads and precordial leads, when present in conjunction with other findings, may be helpful in raising the clinical suspicion of cardiac amyloidosis.
A 69-year-old woman with a history of hypertension and obesity, hospitalized with atypical chest pain, was diagnosed with left ventricular noncompaction. In-hospital monitoring of the cardiac rhythm revealed multiple episodes of atrial tachycardia and one episode of wide complex tachycardia (WCT) with left bundle branch block-like morphology and a right superior QRS axis. The electrocardiographic criteria were suggestive of a supraventricular origin of the WCT. Given the importance of reaching the correct diagnosis when dealing with a WCT, we tried to further define the pattern of ventricular activation using vectorcardiography (VCG). We analyzed the QRS loops during WCT in comparison to a sinus beat, a narrow complex tachycardia beat, and a premature ventricular contraction. The fast initial activation seen in the efferent limb of the QRS loop during the WCT was thought to be reflective of the fast initial activation via the conduction system seen in SVT with aberrancy, which was our final diagnosis for the WCT episode. This case illustrates a novel use of vectorcardiography as an additional diagnostic tool in the differential diagnosis of WCT.
Introduction: Spontaneous coronary artery dissection (SCAD) represents a very rare and poorly understood condition that is gaining recognition as an important cause of myocardial infarction, especially among young women. The pathogenesis of SCAD is not well established yet, but several theories have been proposed.
Case presentation: We report the case of a 25-year-old woman without any history of cardiovascular disease who presented with acute anterior ST-elevation myocardial infarction (STEMI) due to the luminal obstruction generated by an intramural hematoma from a SCAD of the left main coronary artery, which was successfully treated by coronary artery stenting. Additionally, the patient presented anomalies of coronary origins (ACO) with separate emergences of the left anterior descending (LAD) artery from the left coronary cusp and the left circumflex artery (LCX) from the right coronary cusp, with no apparent clinical significance.
Conclusion: SCAD should always be included in the differential diagnosis of young patients presenting with STEMI. In case of prompt diagnosis, SCAD-STEMI patients are successfully treated with percutaneous coronary intervention (PCI). Moreover, it is of vital importance to identify variants of ACO, even without clinical relevance at the moment of the acute event, in order to initiate an appropriate management, since ACO increases the risk of routine PCI.
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