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1.
Acta Biomed ; 92(3): e2021204, 2021 07 01.
Article in English | MEDLINE | ID: covidwho-1404258

ABSTRACT

Cardiovascular diseases (CVDs)  have been the most common cause of death worldwide for decades. Until recently the most affected patients were middle-aged and elderly, predominantly men, with more frequent ST elevation myocardial infarction  (STEMI) caused by obstructive coronary artery disease (CAD). However, in the last two decades we have noticed an increased incidence of ischemia with non-obstructive coronary arteries (INOCA), which includes myocardial infarction with non-obstructive coronary arteries (MINOCA) and non-myocardial infarction syndromes, such as microvascular and vasospastic angina, conditions that have been particularly pronounced in women and young adults - the population we considered low-risky till than. Therefore, it has become apparent that for this group of patients conventional methods of assessing the risk of future cardiovascular (CV) events are no longer specific and sensitive enough. Heart failure with preserved ejection fraction (HFpEF) is another disease, the incidence of which has been rising rapidly during last two decades, and predominantly affects elderly population. Although the etiology and pathophysiology of INOCA and HFpEF are complex and not fully understood, there is no doubt that the underlying cause of both conditions is endothelial dysfunction (ED) which further promotes the development of left ventricular diastolic dysfunction (LVDD). Plasma biomarkers of ED, as well as natriuretic peptides (NPs), have been intensively investigated recently, and some of them have great potential for early detection and better assessment of CV risk in the future.


Subject(s)
Coronary Artery Disease , Heart Failure , Ventricular Dysfunction, Left , Aged , Coronary Artery Disease/etiology , Female , Heart Failure/epidemiology , Heart Failure/etiology , Heart Ventricles , Humans , Male , Middle Aged , Stroke Volume , Ventricular Dysfunction, Left/etiology
2.
Intern Emerg Med ; 16(5): 1231-1237, 2021 08.
Article in English | MEDLINE | ID: covidwho-1293431

ABSTRACT

BACKGROUND: Patients with coronavirus disease 2019 (Covid-19) may experience venous thrombosis while data regarding arterial thrombosis are sparse. METHODS: Prospective multicenter study in 5 hospitals including 373 patients with Covid-19-related pneumonia. Demographic data, laboratory findings including coagulation tests and comorbidities were reported. During the follow-up any arterial or venous thrombotic events and death were registered. RESULTS: Among 373 patients, 75 (20%) had a thrombotic event and 75 (20%) died. Thrombotic events included 41 venous thromboembolism and 34 arterial thrombosis. Age, cardiovascular disease, intensive care unit treatment, white blood cells, D-dimer, albumin and troponin blood levels were associated with thrombotic events. In a multivariable regression logistic model, intensive care unit treatment (Odds Ratio [OR]: 6.0; 95% Confidence Interval [CI] 2.8-12.6; p < 0.001); coronary artery disease (OR: 2.4; 95% CI 1.4-5.0; p = 0.022); and albumin levels (OR: 0.49; 95% CI 0.28-0.87; p = 0.014) were associated with ischemic events. Age, sex, chronic obstructive pulmonary disease, diabetes, heart failure, coronary heart disease, intensive care unit treatment, in-hospital thrombotic events, D-dimer, C-reactive protein, troponin, and albumin levels were associated with mortality. A multivariable Cox regression analysis showed that in-hospital thrombotic events (hazard ratio [HR]: 2.72; 95% CI 1.59-4.65; p < 0.001), age (HR: 1.035; 95% CI 1.014-1.057; p = 0.001), and albumin (HR: 0.447; 95% CI 0.277-0.723; p = 0.001) predicted morality. CONCLUSIONS: Covid-19 patients experience an equipollent rate of venous and arterial thrombotic events, that are associated with poor survival. Early identification and appropriate treatment of Covid-19 patients at risk of thrombosis may improve prognosis.


Subject(s)
COVID-19/complications , Coronary Artery Disease/etiology , Mortality/trends , Thromboembolism/etiology , Aged , Aged, 80 and over , C-Reactive Protein/analysis , COVID-19/epidemiology , Coronary Artery Disease/epidemiology , Female , Fibrin Fibrinogen Degradation Products/analysis , Humans , Intensive Care Units/organization & administration , Intensive Care Units/statistics & numerical data , Kaplan-Meier Estimate , Logistic Models , Male , Middle Aged , Odds Ratio , Proportional Hazards Models , Prospective Studies , Thromboembolism/epidemiology
3.
Cardiol Rev ; 29(3): 143-149, 2021.
Article in English | MEDLINE | ID: covidwho-1148006

ABSTRACT

The coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 has affected the health of people across the globe. Cardiovascular diseases (CVDs) have a significant relationship with COVID-19, both as a risk factor and prognostic indicator, and as a complication of the disease itself. In addition to predisposing to CVD complications, the ongoing pandemic has severely affected the delivery of timely and appropriate care for cardiovascular conditions resulting in increased mortality. The etiology behind the cardiac injury associated with severe acute respiratory syndrome coronavirus-2 is likely varied, including coronary artery disease, microvascular thrombosis, myocarditis, and stress cardiomyopathy. Further large-scale investigations are needed to better determine the underlying mechanism of myocardial infarction and other cardiac injury in COVID-19 patients and to determine the incidence of each type of cardiac injury in this patient population. Telemedicine and remote monitoring technologies can play an important role in optimizing outcomes in patients with established CVD. In this article, we summarize the various impacts that COVID-19 has on the cardiovascular system, including myocardial infarction, myocarditis, stress cardiomyopathy, thrombosis, and stroke.


Subject(s)
COVID-19/physiopathology , Cardiovascular Diseases/physiopathology , COVID-19/complications , COVID-19/epidemiology , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/etiology , Comorbidity , Coronary Artery Disease/epidemiology , Coronary Artery Disease/etiology , Coronary Artery Disease/physiopathology , Coronary Thrombosis/etiology , Coronary Thrombosis/physiopathology , Heart Disease Risk Factors , Humans , Ischemic Stroke/epidemiology , Ischemic Stroke/etiology , Ischemic Stroke/physiopathology , Microvessels , Myocardial Infarction/epidemiology , Myocardial Infarction/etiology , Myocardial Infarction/physiopathology , Myocarditis/etiology , Myocarditis/physiopathology , SARS-CoV-2 , Stroke/epidemiology , Stroke/etiology , Stroke/physiopathology , Takotsubo Cardiomyopathy/etiology , Takotsubo Cardiomyopathy/physiopathology , Thrombosis/etiology , Thrombosis/physiopathology
4.
Pediatr Cardiol ; 42(2): 460-462, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1064453

ABSTRACT

We describe a 16-year-old asymptomatic male who presented with coronary artery dilation (z score + 2.3) identified on echo performed solely for presence of COVID-19 antibodies. This case raises the question of whether cardiac screening should be considered for all patients with a history of COVID-19.


Subject(s)
COVID-19/complications , Coronary Aneurysm/diagnostic imaging , Coronary Artery Disease/diagnostic imaging , Adolescent , Coronary Aneurysm/etiology , Coronary Artery Disease/etiology , Dilatation, Pathologic , Echocardiography , Humans , Male , SARS-CoV-2
5.
Med Hypotheses ; 143: 110125, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-665482

ABSTRACT

The novel coronavirus (SARS-CoV-2) is primarily a respiratory pathogen and its clinical manifestations are dominated by respiratory symptoms, the most severe of which is acute respiratory distress syndrome (ARDS). However, COVID-19 is increasingly recognized to cause an overwhelming inflammatory response and cytokine storm leading to end organ damage. End organ damage to heart is one of the most severe complications of COVID-19 that increases the risk of death. We proposed a two-fold mechanism responsible for causing acute coronary events in patients with COVID-19 infection: Cytokine storm leading to rapid onset formation of new coronary plaques along with destabilization of pre-existing plaques and direct myocardial injury secondary to acute systemic viral infection. A well-coordinated immune response is the first line innate immunity against a viral infection. However, an uncoordinated response and hypersecretion of cytokines and chemokines lead to immune related damage to the human body. Human Coronavirus (HCoV) infection causes infiltration of inflammatory cells that cause excessive production of cytokines, proteases, coagulation factors, oxygen radicals and vasoactive molecules causing endothelial damage, disruption of fibrous cap and initiation of formation of thrombus. Systemic viral infections also cause vasoconstriction leading to narrowing of vascular lumen and stimulation of platelet activation via shear stress. The resultant cytokine storm causes secretion of hypercoagulable tissue factor without consequential increase in counter-regulatory pathways such as AT-III, activated protein C and plasminogen activator type 1. Lastly, influx of CD4+ T-cells in cardiac vasculature results in an increased production of cytokines that stimulate smooth muscle cells to migrate into the intima and generate collagen and other fibrous products leading to advancement of fatty streaks to advanced atherosclerotic lesions. Direct myocardial damage and cytokine storm leading to destabilization of pre-existing plaques and accelerated formation of new plaques are the two instigating mechanisms for acute coronary syndromes in COVID-19.


Subject(s)
Acute Coronary Syndrome/etiology , Betacoronavirus , Coronavirus Infections/complications , Models, Cardiovascular , Pandemics , Pneumonia, Viral/complications , Acute Coronary Syndrome/physiopathology , CD4-Positive T-Lymphocytes/immunology , COVID-19 , Chemokines/physiology , Coronary Artery Disease/etiology , Coronary Artery Disease/physiopathology , Coronary Vessels/metabolism , Coronavirus Infections/immunology , Coronavirus Infections/physiopathology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/physiopathology , Cytokines/physiology , Humans , Immunity, Innate , Plaque, Atherosclerotic/etiology , Plaque, Atherosclerotic/physiopathology , Platelet Activation , Pneumonia, Viral/immunology , Pneumonia, Viral/physiopathology , SARS-CoV-2 , Vasoconstriction , Virus Diseases/complications , Virus Diseases/immunology
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