COVID-19 and Cardiomyopathy: A Systematic Review

Background: Cardiomyopathies (CMPs) due to myocytes involvement are among the leading causes of sudden adolescent death and heart failure. During the COVID-19 pandemic, there are limited data available on cardiac complications in patients with COVID-19, leading to severe outcomes.Methods: We conducted a systematic search in Pubmed/Medline, Web of Science, and Embase databases up to August 2020, for all relevant studies about COVID-19 and CMPs.Results: A total of 29 articles with a total number of 1460 patients were included. Hypertension, diabetes, obesity, hyperlipidemia, and ischemic heart disease were the most reported comorbidities among patients with COVID-19 and cardiomyopathy. In the laboratory findings, 21.47% of patients had increased levels of troponin. Raised D-dimer levels were also reported in all of the patients. Echocardiographic results revealed mild, moderate, and severe Left Ventricular (LV) dysfunction present in 17.13, 11.87, and 10% of patients, respectively.Conclusions: Cardiac injury and CMPs were common conditions in patients with COVID-19. Therefore, it is suggested that cardiac damage be considered in managing patients with COVID-19.

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Association of Cardiac Injury and Malignant Left Ventricular Hypertrophy With Risk of Heart Failure in African Americans

JAMA Cardiology ◽

10.1001/jamacardio.2018.4300 ◽

2019 ◽

Vol 4 (1) ◽

pp. 51 ◽

Cited By ~ 5

Author(s):

Ambarish Pandey ◽

Neil Keshvani ◽

Colby Ayers ◽

Adolfo Correa ◽

Mark H. Drazner ◽

...

Keyword(s):

Heart Failure ◽

African Americans ◽

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Cardiac Injury ◽

Left Ventricular

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Abstract 15848: Restoration of Normal Cardiomyocyte Basal and β-Adrenergic Receptor (AR) Subtype Modulation in Heart Failure by Chronic Phosphodiesterase Type 5 Inhibition With Sildenafil

Circulation ◽

10.1161/circ.130.suppl_2.15848 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Tiankai Li ◽

Heng-Jie Cheng ◽

Shadi A Qasem ◽

Michael Callahan ◽

Wei-Min Li ◽

...

Keyword(s):

Heart Failure ◽

Adrenergic Receptor ◽

Pde5 Inhibitor ◽

Left Ventricular ◽

Cell Contractility ◽

Lv Dysfunction ◽

Myocyte Function ◽

Phosphodiesterase Type ◽

Β Adrenergic Receptors ◽

Mini Pump

Background: We have shown that Sildenafil (SIL), a selective PDE5 inhibitor reversed left ventricular (LV) dysfunction and β- adrenergic receptors (AR) desensitization in heart failure (HF). However the mechanism is not yet clear. Recent evidence suggests that normal myocardial performance depend on the balance in cardiomyocyte β 3 -, β 1 -, and β 2 -AR. Pivotal restructuring of β-AR system resulting in decline of β-adrenergic reserve plays a crucial role in the development of HF. We assessed the hypothesis that chronic SIL would prevent HF-induced abnormalities of β-AR subtype-stimulated regulation on intrinsic LV myocyte function and [Ca 2+ ] i regulation, thus restoring cardiac function. Methods: Studies were conducted in 3 groups (10/group) of rats: 1) HF, 12 weeks (W) after receiving isoproterenol (ISO) (170 mg/kg sq for 2 days); 2) HF/SIL, 8W after receiving ISO, SIL (70 μg/kg/day sq via mini pump) was initiated and given for 1 M; and 3) controls. After 12W, we compared LV myocyte contractile and [Ca 2+ ] iT responses to β-AR subtype stimulation by random exposure of myocytes to ISO (10 -8 M) or a selective β 1 -, β 2 -, or β 3 -agonist, Norepinephrine (NE, 10 -7 M), Zinterol (ZIN, 10 -5 M) and BRL-37,344 (BRL, 10 -8 M), respectively, during drug superfusion. Results: Only ISO-treated rats had HF showed 46% decreased LV contractility (E ES ) and extensive LV myocardium fibrosis. Compared with normal myocytes (N), in HF myocytes, basal cell contractility (dL/dt max , HF: 77 vs N: 136 μm/s), relaxation and [Ca 2+ ] iT all significantly decreased. ISO-stimulated dL/dt max (31% vs 67%) was attenuated accompanied by a diminished NE-mediated increase in dL/dt max (13% vs 49%), but enhanced BRL-induced decreases in dL/dt max (-29% vs -16%).The response of dL/dt max (25% vs 15%) to ZIN was increased. Importantly, in HF/SIL myocytes, the basal dL/dt max (139 μm/s) and [Ca 2+ ] iT remained close to control values with preserved β-stimulated positive modulation on cell contraction. The increases in dL/dt max in response to ISO (70%) and NE (44%) were similar as in normal myocytes, but repose to ZIN (27%) was enhanced. Conclusions: Chronic SIL reverses β-adrenergic signaling defects, resensitizing the β-AR subtype system modulation on LV myocytes function, thus playing a salutary role in HF.

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Renovascular hypertension induces myocardial mitochondrial damage, contributing to cardiac injury and dysfunction in pigs with metabolic syndrome

American Journal of Hypertension ◽

10.1093/ajh/hpaa202 ◽

2020 ◽

Author(s):

Arash Aghajani Nargesi ◽

Mohamed C Farah ◽

Xiang-Yang Zhu ◽

Lei Zhang ◽

Hui Tang ◽

...

Keyword(s):

Metabolic Syndrome ◽

Renovascular Hypertension ◽

Cardiac Fibrosis ◽

Cardiac Injury ◽

Left Ventricular ◽

Mitochondrial Damage ◽

Mitochondrial Morphology ◽

H2o2 Production ◽

Cardiac Damage ◽

Cardiovascular Morbidity And Mortality

Abstract Background Subjects with renovascular hypertension (RVH) often manifest with metabolic syndrome (MetS) as well. Coexisting MetS and hypertension increases cardiovascular morbidity and mortality, but the mechanisms underlying cardiac injury remain unknown. We hypothesized that superimposition of MetS induces myocardial mitochondrial damage, leading to cardiac injury and dysfunction in swine RVH. Methods Pigs were studied after 16 weeks of diet-induced MetS with or without RVH (unilateral renal artery stenosis), and Lean controls (n=6 each). Systolic and diastolic cardiac function were assessed by multi-detector CT, and cardiac mitochondrial morphology (transmission electron microscopy) and myocardial function in tissue and isolated mitochondria. Results Body weight was similarly higher in MetS groups vs. Lean. RVH groups achieved significant stenosis and developed hypertension. Mitochondrial matrix density and ATP production were lower and H2O2 production higher in RVH groups versus Lean and MetS. Lean+RVH (but not MetS+RVH) activated mitophagy, which was associated with decreased myocardial expression of mitophagy-related microRNAs. MetS groups exhibited higher numbers of inter-mitochondrial junctions (IMJs), which could have prevented membrane depolarization/activation of mitophagy in MetS+RVH. Cardiac fibrosis, hypertrophy (increased left ventricular muscle mass), and diastolic function (decreased E/A ratio) were greater in MetS+RVH versus Lean+RVH. Conclusions Superimposition of MetS on swine RVH induces myocardial mitochondrial damage and dysfunction. MetS+RVH failed to activate mitophagy, resulting in greater cardiac remodeling, fibrosis, and diastolic dysfunction. Mitochondrial injury and impaired mitophagy may constitute important mechanisms and potential therapeutic targets to ameliorate cardiac damage and dysfunction in patients with coexisting MetS and RVH.

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Association of fibrinogen and D‑dimer levels with severity of acute coronary syndromes

Journal of Rare Cardiovascular Diseases ◽

10.20418/jrcd.v0i0.409.g327 ◽

2020 ◽

Author(s):

Mukhyaprana M. Prabhu ◽

Jagadish Madireddy ◽

Ranjan K. Shetty ◽

Weena Stanley

Keyword(s):

Acute Coronary Syndromes ◽

Pearson Correlation ◽

Characteristic Curve ◽

Left Ventricular ◽

Mortality And Morbidity ◽

Lv Dysfunction ◽

Coronary Syndromes ◽

The Mean ◽

A Prospective Study ◽

D Dimer

Background: Acute coronary syndromes (ACSs) are the primary cause of mortality worldwide. The aim of the study was to assess the as‑sociations of serum fibrinogen and plasma D‑dimer levels with angiographic severity of atherosclerotic lesions as well as the presence of in‑hospital complications and complications at 30‑day follow‑up in patients with ACS. Methods: This was a prospective study including 107 patients with ACS. Severity of CAD was assessed by the Gensini score. Correlations of D‑dimer and fibrinogen levels with complica‑tions such as heart failure, arrhythmia, recurrent angina, and cardiac death were assessed using the Pearson correlation coefficient and the receiver operating characteristic curve analysis. Results: The mean age of patients was 61±10.9 years. Mean serum fibrinogen levels were higher in individuals with severe left ventricular (LV) dysfunction than in those with moderate and mild LV dysfunction (444 mg/dl, 404 mg/dl, and 330 mg/dl, respectively). Similarly, the mean plasma D‑dimer level was higher in individuals with severe ACS (1.03 μg/ml) than in those with moderate (1.88 μg/ml) and mild ACS (3.5 μg/ml). Conclusion: Our study revealed that patients with higher serum fibrinogen levels tend to have more severe ACS, greater LV dysfunction, and a higher rate of complications. Therapies aimed at reducing fibrinogen levels might help reduce mortality and morbidity in patients with ACS.

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Abstract 16344: Pericardial Complications in Patients With COVID-19: A Systematic Review of Published Cases

Circulation ◽

10.1161/circ.142.suppl_3.16344 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Sandeep Singh ◽

Akhil Jain ◽

Priyanka Chaudhari ◽

Faizan Ahmad Malik ◽

Virmitra Desai ◽

...

Keyword(s):

Heart Failure ◽

Pericardial Effusion ◽

Cardiac Tamponade ◽

Troponin I ◽

Case Reports ◽

Cardiac Injury ◽

Pericardial Tamponade ◽

Time Interval ◽

Cardiac Damage ◽

St Segment Elevation

Introduction: COVID-19 has been linked to cardiac damage and life-threatening pericardial complication on which data are trivial which incited us to perform this review of published case reports. Methods: PubMed/Medline, Web of Science and SCOPUS were searched until June 2020 for case reports on COVID-19-associated pericarditis, cardiac tamponade or pericardial effusion. Results: We identified 8 articles reporting 11 COVID-19 positive cases [mean age: 51.4±14.3 (34-78 yrs) 5 male/6 female)] with pericardial complications. All (100%) cases were COVID-19 positive at the presentation with ~80% having dyspnea, chest pain and cough. Time interval from first symptom to pericardial effusion was 7±8 (1-26) days. Five patients reported heart failure with reduced EF on echocardiography with mean LVEF 36.25%±8.54%. All patients showed nearly normal Troponin-I without angiographically significant stenosis except one. Out of 8 cases on echocardiography 4 cases reported with diffuse hypokinesia, 2 reported inferior and inferolateral walls hypokinesia and 2 reported signs of pericardial tamponade. Out of 11 patients, cardiovascular risk factors in the form of diabetes or hypertension or obesity were present in 5 patients. Cardiovascular comorbidities such as heart failure with low ejection fraction, non-ischemic cardiomyopathy and prior myocarditis were present in 3 patients. ST-segment elevation in 3, sinus tachycardia in 2, T wave inversion in 1 case were noted. Four patients developed cardiac tamponade, 1 developed takotsubo syndrome and 3 patients died. Conclusions: COVID-19 patients had signs of a high burden of cardiac injury. Pericardial complications (pericardial effusion and cardiac tamponade) remain infrequent complications which may require prompt care to avoid mortality.

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Clinical characteristics of 113 deceased patients with coronavirus disease 2019: retrospective study

BMJ ◽

10.1136/bmj.m1091 ◽

2020 ◽

pp. m1091 ◽

Cited By ~ 1031

Author(s):

Tao Chen ◽

Di Wu ◽

Huilong Chen ◽

Weiming Yan ◽

Danlei Yang ◽

...

Keyword(s):

Heart Failure ◽

Acute Respiratory Distress Syndrome ◽

Respiratory Failure ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Clinical Characteristics ◽

Distress Syndrome ◽

Cardiac Injury ◽

Cardiac Complications ◽

Type I

Abstract Objective To delineate the clinical characteristics of patients with coronavirus disease 2019 (covid-19) who died. Design Retrospective case series. Setting Tongji Hospital in Wuhan, China. Participants Among a cohort of 799 patients, 113 who died and 161 who recovered with a diagnosis of covid-19 were analysed. Data were collected until 28 February 2020. Main outcome measures Clinical characteristics and laboratory findings were obtained from electronic medical records with data collection forms. Results The median age of deceased patients (68 years) was significantly older than recovered patients (51 years). Male sex was more predominant in deceased patients (83; 73%) than in recovered patients (88; 55%). Chronic hypertension and other cardiovascular comorbidities were more frequent among deceased patients (54 (48%) and 16 (14%)) than recovered patients (39 (24%) and 7 (4%)). Dyspnoea, chest tightness, and disorder of consciousness were more common in deceased patients (70 (62%), 55 (49%), and 25 (22%)) than in recovered patients (50 (31%), 48 (30%), and 1 (1%)). The median time from disease onset to death in deceased patients was 16 (interquartile range 12.0-20.0) days. Leukocytosis was present in 56 (50%) patients who died and 6 (4%) who recovered, and lymphopenia was present in 103 (91%) and 76 (47%) respectively. Concentrations of alanine aminotransferase, aspartate aminotransferase, creatinine, creatine kinase, lactate dehydrogenase, cardiac troponin I, N-terminal pro-brain natriuretic peptide, and D-dimer were markedly higher in deceased patients than in recovered patients. Common complications observed more frequently in deceased patients included acute respiratory distress syndrome (113; 100%), type I respiratory failure (18/35; 51%), sepsis (113; 100%), acute cardiac injury (72/94; 77%), heart failure (41/83; 49%), alkalosis (14/35; 40%), hyperkalaemia (42; 37%), acute kidney injury (28; 25%), and hypoxic encephalopathy (23; 20%). Patients with cardiovascular comorbidity were more likely to develop cardiac complications. Regardless of history of cardiovascular disease, acute cardiac injury and heart failure were more common in deceased patients. Conclusion Severe acute respiratory syndrome coronavirus 2 infection can cause both pulmonary and systemic inflammation, leading to multi-organ dysfunction in patients at high risk. Acute respiratory distress syndrome and respiratory failure, sepsis, acute cardiac injury, and heart failure were the most common critical complications during exacerbation of covid-19.

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SR Ca(2+)-ATPase activity and expression in ventricular myocardium of dogs with heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.273.1.h12 ◽

1997 ◽

Vol 273 (1) ◽

pp. H12-H18 ◽

Cited By ~ 7

Author(s):

R. C. Gupta ◽

H. Shimoyama ◽

M. Tanimura ◽

R. Nair ◽

M. Lesch ◽

...

Keyword(s):

Heart Failure ◽

Atpase Activity ◽

Sodium Dodecyl ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Maximal Velocity ◽

Protein Levels ◽

Lv Dysfunction ◽

Lv Ejection Fraction ◽

Tissue Specimens

The purpose of this study was to examine the activity and expression of sarcoplasmic reticulum (SR) Ca(2+)-ATPase in left ventricular (LV) myocardium of dogs with chronic heart failure (HF). LV and right ventricular (RV) tissue specimens were obtained from six normal (NL) control dogs and six dogs with chronic HF (LV ejection fraction, 23 +/- 2%) produced by multiple sequential intracoronary microembolizations. Thapsigargin-sensitive Ca(2+)-ATPase activity was measured in isolated SR membrane fractions prepared from LV and RV myocardium. Ca(2+)-ATPase expression, using a specific dog myocardium monoclonal antibody, was measured in sodium dodecyl sulfate (SDS) extract prepared from LV and RV myocardium. Ca(2+)-ATPase activity in both ventricles of NL or HF dogs increased with increasing Ca2+ concentration and reached a plateau at 3 microM Ca2+. The maximal velocity (Vmax, mumol Pi released.min-1.mg-1) of Ca(2+)-ATPase activity was significantly lower in LV of HF dogs compared with NL (0.15 +/- 0.01 vs. 0.23 +/- 0.01, P < 0.05), whereas the affinity of the Ca2+ pump for Ca2+ was unchanged. LV tissue levels of Ca(2+)-ATPase (densitometric units/5 micrograms noncollagen protein) were also significantly lower in LV myocardium of HF dogs compared with NL (3.52 +/- 0.43 vs. 5.53 +/- 0.47, P < 0.05). No significant differences in Ca(2+)-ATPase activity or expression were observed in RV myocardium of HF dogs compared with NL. We conclude that SR Ca(2+)-ATPase activity and protein levels are reduced in LV myocardium of dogs with chronic HF. This abnormality of the SR Ca2+ pump of the failed LV can result in impaired Ca2+ uptake and ultimately to Ca2+ overload and global LV dysfunction.

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Differential atrial and ventricular expression of myocardial BNP during evolution of heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1998.274.5.h1684 ◽

1998 ◽

Vol 274 (5) ◽

pp. H1684-H1689 ◽

Cited By ~ 39

Author(s):

Andreas Luchner ◽

Tracy L. Stevens ◽

Daniel D. Borgeson ◽

Margaret Redfield ◽

Chi-Ming Wei ◽

...

Keyword(s):

Gene Expression ◽

Heart Failure ◽

Arterial Pressure ◽

Left Atrium ◽

Limit Of Detection ◽

Tissue Concentration ◽

Ventricular Myocardium ◽

Left Ventricular ◽

Lv Function ◽

Lv Dysfunction

Although brain natriuretic peptide (BNP) of myocardial origin is important in cardiovascular and renal function and as a marker of cardiac dysfunction, the expression of BNP in atrial and ventricular myocardium remains controversial both under normal conditions and in heart failure. We therefore determined left atrial and left ventricular (LV) gene expression and tissue concentration as well as circulating BNP during the evolution of rapid ventricular pacing-induced congestive heart failure (CHF) in the dog. Early LV dysfunction after 10 days of pacing was characterized by impaired LV function but maintained arterial pressure, and overt CHF after 38 days of pacing was characterized by further impaired LV function and decreased systemic arterial pressure. Under normal conditions, cardiac BNP mRNA and cardiac tissue BNP were of atrial origin. In early LV dysfunction, BNP mRNA and tissue BNP were markedly increased in the left atrium in association with an increase in circulating BNP but remained below or at the limit of detection in the LV. In overt CHF, BNP mRNA was further increased in the left atrium and first increased in the LV, together with an increase in LV tissue BNP and a further increase in circulating BNP. In the progression of CHF, early LV dysfunction is characterized by a selective increase in atrial BNP expression in association with increased circulating BNP. Overt CHF is characterized by an additional recruitment of ventricular BNP expression and a further increase in circulating BNP. These studies provide important new insight into the local and temporal regulation of cardiac BNP gene expression during the progression of heart failure and underscore the predominant endocrine role of atrial myocardium under normal conditions and in early LV dysfunction.

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Butein Inhibits Oxidative Stress Injury in Rats with Chronic Heart Failure via ERK/Nrf2 Signaling

Cardiovascular Therapeutics ◽

10.1155/2022/8684014 ◽

2022 ◽

Vol 2022 ◽

pp. 1-10

Author(s):

Peng Liu ◽

Quanli Pan

Keyword(s):

Oxidative Stress ◽

Heart Failure ◽

Chronic Heart Failure ◽

Rat Model ◽

Myocardial Dysfunction ◽

Cardiac Injury ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Stress Injury ◽

Oxidative Stress Injury

Background. Chronic heart failure (CHF) is a serious heart disease resulting from cardiac dysfunction. Oxidative stress is an important factor in aging and disease. Butein, however, has antioxidant properties. To determine the effect of butein on oxidative stress injury in rats, a CHF rat model was established. Methods. The CHF rat model was induced by abdominal aortic coarctation (AAC). Rats in CHF+butein and sham+butein group were given 100 mg/kg butein via gavage every day to detect the effect of butein on oxidative stress injury and myocardial dysfunction. The cardiac structural and functional parameters, including the left ventricular end-systolic dimension (LVESD), the left ventricular end-diastolic dimension (LVEDD), the left ventricular ejection fraction (LVEF), and the left ventricular fractional shortening (LVFS), were measured. Oxidative stress was measured through the production of reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA). Cardiac injury markers like creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) were evaluated. Hematoxylin and eosin (H&E) staining was used to observe the myocardial cell morphology. The effect of butein on the extracellular signal-regulated kinase (ERK)/nuclear factor-E2 p45-related factor (Nrf2) signaling was confirmed by Western blot analysis. Results. Butein had a significant effect on CHF in animal models. In detail, butein inhibited oxidative stress, relieved cardiac injury, and alleviated myocardial dysfunction. Importantly, butein activated the ERK1/2 pathway, which contributed to Nrf2 activation and subsequent heme oxygenase-1 (HO-1) and glutathione cysteine ligase regulatory subunit (GCLC) induction. Conclusions. In this study, butein inhibits oxidative stress injury in CHF rat model via ERK/Nrf2 signaling pathway.

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Cloud Connected Non-Invasive Medical Device for Instant Left Ventricular Dysfunction Assessment via Any Smartphone (Preprint)

10.2196/preprints.11880 ◽

2018 ◽

Author(s):

Mark Skowronski ◽

Kaustubh Kale ◽

Steven Borzak ◽

Robert Chait

Keyword(s):

Heart Failure ◽

Ejection Fraction ◽

Medical Device ◽

Gold Standard ◽

Left Ventricular ◽

Assessment System ◽

Lv Function ◽

Time Intervals ◽

Cardiac Time Intervals ◽

Lv Dysfunction

BACKGROUND Left Ventricular (LV) dysfunction is the inability of the heart to effectively pump blood through the circulatory system, leading to compensation and eventually heart failure (HF). Ninety-one million American adults with predisposing conditions are at risk for HF and need better screening and diagnosis to prevent disease progression, and 24 million Americans with diagnosed HF need better monitoring to reduce the high hospital readmission rates (25% within 30 days; 50% within 6 months). This epidemic of HF is causing a significant burden on our health care system, with $20 billion in direct medical cost related to HF and $1 billion in in-patient hospital costs annually. Clinical interventions based on standard measurements (blood pressure, weight, electrocardiograms) have not demonstrated a significant reduction in readmissions or all-cause mortality within 180 days after enrollment. Successful treatment may be determined from 2D transthoracic echocardiography (echo) or right heart catherization, but these gold standard methods have limitations of cost, accessibility, and availability of sonographers and cardiologists. An alternative is the HEMOTAG CardioPulmonary Assessment System (CPAS), a new cloud-connected medical device that delivers cardiac time intervals comparable to the gold standard measurements of an echo from an easy-to-use, noninvasive device accessible via any smartphone. OBJECTIVE Given the clinical and economic impact of LV dysfunction and in view of the cost and accessibility of existing devices, there is a need for accurate, absolute, and actionable measurements, available instantly through a noninvasive and easy-to-use system. With the ability of provide rapid assessment of LV dysfunction in adults, keeping patients healthy and safe. The objective of the current study was to compare HEMOTAG to an echo for accuracy in assessment of LV dysfunction, using heart sounds and an ECG signal transduced via 3 thoracic electrodes. METHODS One hundred twenty-three consecutive patients undergoing 2D transthoracic echocardiograms were recruited at an outpatient cardiology clinic from March 2016 through February 2017. Conventional echo variables and cardiac time intervals were assessed, and all patients were analyzed using HEMOTAG which recorded multi-channel acoustic and ECG data. LV dysfunction was assessed using the 2016 American Society of Echocardiography (ASE) standard and compared to cardiac time intervals from HEMOTAG. Patients were separated by age for comparisons. HEMOTAG indices were then assessed to identify normal/abnormal LV function. RESULTS ASE diagnoses: 46 normal, 21 heart failure with preserved ejection fraction (HFpEF), 15 heart failure with reduced ejection fraction (HFrEF), and 41 indeterminate patients. HFrEF was defined as EF <53%, and systolic time ratio (STR=pre-ejection period/ejection time). 0.3 was a sensitive measure for detecting reduced EF as in HFrEF. Detecting EF <53% in patients older than 60: HEMOTAG STR sensitivity=65%, specificity=80%, AUC=.765; Echo STR sensitivity=85%, specificity=80%, AUC=0.895. CONCLUSIONS HEMOTAG represents a potentially widely applicable technology for the assessment of LV dysfunction via a noninvasive approach, providing absolute assessment (without requiring certified technicians to operate or interpretation of an echo) and enabling rapid, real-time, anywhere, anytime assessment of LV dysfunction.

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