66 research outputs found

    Is It Antiphospholipid Syndrome?

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    The diagnosis of bacterial endocarditis remains a challenge, as nearly half of cases develop in the absence of preexistent heart disease and known risk factors. Not infrequently, a blunted clinical course at onset can lead to erroneous diagnoses. We present the case of a 47-year-old previously healthy man in which a presumptive diagnosis of antiphospholipid syndrome was made based on the absence of echocardiographically detected heart involvement, a negative blood culture, normal C-reactive protein (CRP) levels, a positive lupus anticoagulant (LAC) test, and evidence of splenic infarcts. The patient eventually developed massive aortic endocarditic involvement, with blood cultures positive for Streptococcus bovis, and was referred for valvular replacement. This case not only reminds us of the diagnostic challenges of bacterial endocarditis, but also underlines the need for a critical application of antiphospholipid syndrome diagnostic criteria

    Contribution of Autonomic Reflexes to the Hyperadrenergic State in Heart Failure

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    Heart failure (HF) is a complex syndrome representing the clinical endpoint of many cardiovascular diseases of different etiology. Given its prevalence, incidence and social impact, a better understanding of HF pathophysiology is paramount to implement more effective anti-HF therapies. Based on left ventricle (LV) performance, HF is currently classified as follows: (1) with reduced ejection fraction (HFrEF); (2) with mid-range EF (HFmrEF); and (3) with preserved EF (HFpEF). A central tenet of HFrEF pathophysiology is adrenergic hyperactivity, featuring increased sympathetic nerve discharge and a progressive loss of rhythmical sympathetic oscillations. The role of reflex mechanisms in sustaining adrenergic abnormalities during HFrEF is increasingly well appreciated and delineated. However, the same cannot be said for patients affected by HFpEF or HFmrEF, whom also present with autonomic dysfunction. Neural mechanisms of cardiovascular regulation act as "controller units," detecting and adjusting for changes in arterial blood pressure, blood volume, and arterial concentrations of oxygen, carbon dioxide and pH, as well as for humoral factors eventually released after myocardial (or other tissue) ischemia. They do so on a beat-to-beat basis. The central dynamic integration of all these afferent signals ensures homeostasis, at rest and during states of physiological or pathophysiological stress. Thus, the net result of information gathered by each controller unit is transmitted by the autonomic branch using two different codes: intensity and rhythm of sympathetic discharges. The main scope of the present article is to (i) review the key neural mechanisms involved in cardiovascular regulation; (ii) discuss how their dysfunction accounts for the hyperadrenergic state present in certain forms of HF; and (iii) summarize how sympathetic efferent traffic reveal central integration among autonomic mechanisms under physiological and pathological conditions, with a special emphasis on pathophysiological characteristics of HF

    Prognostic Value of 12-Leads Electrocardiogram at Emergency Department in Hospitalized Patients with Coronavirus Disease-19

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    BackgroundElectrocardiogram (ECG) offers a valuable resource easily available in the emergency setting.ObjectiveAim of the study was to describe ECG alterations on emergency department (ED) presentation or that developed during hospitalization in SARS-CoV-2-infected patients and their association with 28-day mortality.MethodsA retrospective, single-center study including hospitalized patients with SARS-CoV-2 was conducted. ECG was recorded on ED admission to determine: heart rhythm, rate, and cycle; atrio-ventricular and intra-ventricular conduction; right ventricular strain; and ventricular repolarization. A specialized cardiologist blinded for the outcomes performed all 12-lead ECG analyses and their interpretation.Results190 patients were included, with a total of 24 deaths (12.6%). Age (p < 0.0001) and comorbidity burden were significantly higher in non-survivors (p < 0.0001). Atrial fibrillation (AF) was more frequent in non-survivors (p < 0.0001), alongside a longer QTc interval (p = 0.0002), a lower Tp-e/QTc ratio (p = 0.0003), and right ventricular strain (p = 0.013). Remdesivir administration was associated with bradycardia development (p = 0.0005) but no increase in mortality rates. In a Cox regression model, AF (aHR 3.02 (95% CI 1.03-8.81); p = 0.042), QTc interval above 451 ms (aHR 3.24 (95% CI 1.09-9.62); p = 0.033), and right ventricular strain (aHR 2.94 (95% CI 1.01-8.55); p = 0.047) were associated with higher 28-day mortality risk.ConclusionsQTc interval > 451 ms, right ventricular strain, and AF are associated with higher mortality risk in SARS-CoV-2 hospitalized patients. ECG recording and its appropriate analysis offers a simple, quick, non-expensive, and validated approach in the emergency setting to guide COVID-19 patients' stratification

    Prognostic factors associated with mortality risk and disease progression in 639 critically ill patients with COVID-19 in Europe: Initial report of the international RISC-19-ICU prospective observational cohort

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    Right Ventricular Longitudinal Strain

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    Case Report Is It Antiphospholipid Syndrome?

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    The diagnosis of bacterial endocarditis remains a challenge, as nearly half of cases develop in the absence of preexistent heart disease and known risk factors. Not infrequently, a blunted clinical course at onset can lead to erroneous diagnoses. We present the case of a 47-year-old previously healthy man in which a presumptive diagnosis of antiphospholipid syndrome was made based on the absence of echocardiographically detected heart involvement, a negative blood culture, normal C-reactive protein (CRP) levels, a positive lupus anticoagulant (LAC) test, and evidence of splenic infarcts. The patient eventually developed massive aortic endocarditic involvement, with blood cultures positive for Streptococcus bovis, and was referred for valvular replacement. This case not only reminds us of the diagnostic challenges of bacterial endocarditis, but also underlines the need for a critical application of antiphospholipid syndrome diagnostic criteria

    Bedside echocardiography in internal medicine: which are the key questions and answers for our decision-making?

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    The advent of portable equipment in the last years has brought ultrasound (US) technology available at patient bedside, giving the opportunity to non-cardiologists to extend cardiac assessment based on physical examination. Bedside echocardiography is a question-driven examination, where simple and often dichotomous answers are searched. It is performed using phased-array probes and bi-dimensional images are visually evaluated to obtain information regarding cardiac size and function, presence of pericardial effusion, gross valvular diseases. Although this approach cannot in any case substitute a standard 2D color-Doppler echocardiography, bedside echocardiography has been demonstrated to maintain a good diagnostic accuracy when limited to basic questions, even in the hands of short-trained non cardiologist physicians. At present the bedside US approach is widely used in different settings and focused echocardiography takes part together with US explorations of lung, abdomen and deep veins in an integrated perspective that perfectly fits with the holistic approach of the internist. In this context we address two typical scenarios encountered in the internal medicine divisions - the patient presenting with dyspnea or nonpost- traumatic hypotension - showing the main questions we can ask to bedside echocardiography for a rapid identification of the determinants of symptoms and consequently for a therapeutic choice based on more objective evidence

    Modeling the cardiac response to hemodynamic changes associated with COVID-19: a computational study

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    Emerging studies address how COVID-19 infection can impact the human cardiovascular system. This relates particularly to the development of myocardial injury, acute coronary syndrome, myocarditis, arrhythmia, and heart failure. Prospective treatment approach is advised for these patients. To study the interplay between local changes (reduced contractility), global variables (peripheral resistances, heart rate) and the cardiac function, we considered a lumped parameters computational model of the cardiovascular system and a three-dimensional multiphysics model of cardiac electromechanics. Our mathematical model allows to simulate the systemic and pulmonary circulations, the four cardiac valves and the four heart chambers, through equations describing the underlying physical processes. By the assessment of conventionally relevant parameters of cardiac function obtained through our numerical simulations, we propose a computational model to effectively reveal the interactions between the cardiac and pulmonary functions in virtual subjects with normal and impaired cardiac function at baseline affected by mild or severe COVID-19
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