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2.
Monaldi Arch Chest Dis ; 2022 Jun 23.
Article in English | MEDLINE | ID: covidwho-2254121

ABSTRACT

Lots of meta-analysis emphasize that a great number of hospitalized patients with moderate and severe forms of COVID-19 developed acute myocardial damage, defined as an increase of cardiac biomarkers, such N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), creatine kinase-myocardial band (CK-MB) and of all type of troponins. The highest mortality rate is related with progressively increasing biomarkers levels and with a history of cardiovascular disease. In fact, the biomarkers dosage should be considered as a prognostic marker in all patients with COVID-19 disease at admission, during hospitalization and in the case of clinical deterioration. The purpose of this review is to evaluate cardiovascular prognostic factors in COVID-19 disease throughout the analysis of cardiac biomarkers to early identify the most serious patients and to optimize their outcomes.

3.
Monaldi Arch Chest Dis ; 92(4)2022 Feb 17.
Article in English | MEDLINE | ID: covidwho-1707772

ABSTRACT

It has been widely reported that the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) attaches human cells by using the Angiotensin Converting Enzyme 2 (ACE2) receptor, but vascular impairment described during coronavirus disease 2019 (COVID-19) infection is primarily due to the direct involvement of the endothelial cells by the virus or secondarily to the inflammatory host response is currently unknown. We therefore aimed to demonstrate in vivo the presence of endothelial dysfunction in six COVID-19 patients without cardiovascular risk factors or pre-existing cardiac condition, using the Endo-PAT 2000, a device able to measure endothelial vasodilation function in a rapid and non-invasive way. Four patients were positive for endothelial dysfunction, with RHI values between 1.13-1.56 (average value 1.32, normal values >1.67); in one of the two negative patients the reported RHI value was slightly above the cutoff (1.72). Our findings confirm that COVID-19 patients are at higher risk of developing endothelial dysfunction. In addition, our results demonstrate that endothelial impairment may occur even in the absence of cardiovascular risk factors.


Subject(s)
COVID-19 , Vascular Diseases , Angiotensin-Converting Enzyme 2 , Endothelial Cells , Humans , Peptidyl-Dipeptidase A , SARS-CoV-2
4.
European heart journal supplements : journal of the European Society of Cardiology ; 23(Suppl G), 2021.
Article in English | EuropePMC | ID: covidwho-1601888

ABSTRACT

Aims COVID-19 has been associated with acute cardiac complications including cardiac arrhythmias. We aimed to assess the prevalence of long-term cardiac arrhythmias in patients recovering from severe COVID-19 infection with proved or suspected of cardiac involvement. Methods and results All patients with COVID-19 infection discharged from the cardiology department of our institution from the 1 March to the 30 April 2020 were considered eligible for this study. Patients were fitted out with an adhesive patch and a wireless single-lead 24-h electrocardiogram (ECG) Holter monitor (Rooti Rx® System, Rooti Labs Ltd, Taipei, Taiwan). RootiRx® is a small device consisting of an integrated sensor system, a microelectronic board with memory storage, and an internal rechargeable battery. This system can provide continuous ECG and was set to monitor heart rhythm for 24 h. The Holter system provides also blood pressure measurements and sleep apnea data which are evaluated through chest wall motion/cyclic variation of heart rate and reported along with the sleep efficiency (percentage of time spent asleep while in bed). Arrhythmic findings, sleep apnea detections, and residual COVID-19 symptoms were reported. The study follow-up was performed 174 (range = 166–190) days after hospital discharge in a cohort of 63 (76% males, median age 66 years) patients. New diagnosis of atrial fibrillation (AF) was performed in three sinus rhythm patients (4.8%). Eleven (18%) patients had asymptomatic bradycardia (<45 b.p.m.) with no pauses lasting more than 3 s. Non-sustained ventricular tachycardia (<30 s) episodes were recorded in two (3.2%) patients, while no sustained ventricular arrhythmia was documented. The Holter system indicated the presence of moderate-to-severe obstructive sleep apnea episodes in 33 (53%) patients without known history of sleep disorders. Some previously unrecognized long-lasting COVID-19 symptoms were also described: fatigue (10, 16%), myalgia (3, 4.8%), and impaired attention (1, 1.6%). Conclusions Six months after the infection, we performed new diagnoses of AF in patients who recovered from severe COVID-19 infection with proved or suspected cardiac involvement using 24-h Holter monitoring. No other arrhythmias were observed, but the Holter system identified obstructive sleep apnea episodes in half of the patients. A relevant percentage of patients also described persisting symptoms of COVID-19 infection. These findings suggest further prospective studies to better describe long-term arrhythmic manifestations and residual symptoms in patients hospitalized with COVID-19 infection.

5.
Rev Cardiovasc Med ; 22(2): 277-286, 2021 06 30.
Article in English | MEDLINE | ID: covidwho-1310348

ABSTRACT

Emerging evidences prove that the ongoing pandemic of coronavirus disease 2019 (COVID-19) is strictly linked to coagulopathy even if pneumonia appears as the major clinical manifestation. The exact incidence of thromboembolic events is largely unknown, so that a relative significant number of studies have been performed in order to explore thrombotic risk in COVID-19 patients. Cytokine storm, mediated by pro-inflammatory interleukins, tumor necrosis factor α and elevated acute phase reactants, is primarily responsible for COVID-19-associated hypercoagulopathy. Also comorbidities, promoting endothelial dysfunction, contribute to a higher thromboembolic risk. In this review we aim to investigate epidemiology and clarify the pathophysiological pathways underlying hypercoagulability in COVID-19 patients, providing indications on the prevention of thromboembolic events in COVID-19. Furthermore we aim to reassume the pathophysiological paths involved in COVID-19 infection.


Subject(s)
Blood Coagulation , COVID-19/blood , Pulmonary Embolism/blood , Venous Thromboembolism/blood , Venous Thrombosis/blood , Anticoagulants/therapeutic use , Blood Coagulation/drug effects , COVID-19/diagnosis , COVID-19/epidemiology , Host-Pathogen Interactions , Humans , Prognosis , Pulmonary Embolism/epidemiology , Pulmonary Embolism/prevention & control , Pulmonary Embolism/virology , Risk Assessment , Risk Factors , SARS-CoV-2/pathogenicity , Venous Thromboembolism/epidemiology , Venous Thromboembolism/prevention & control , Venous Thromboembolism/virology , Venous Thrombosis/epidemiology , Venous Thrombosis/prevention & control , Venous Thrombosis/virology , COVID-19 Drug Treatment
6.
J Med Cases ; 11(7): 207-210, 2020 Jul.
Article in English | MEDLINE | ID: covidwho-1227202

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is mainly responsible for respiratory involvement but cardiac complications are also reported. Nevertheless, potential life-threatening conditions in young people have not been described. A 19-year-old male autistic patient was admitted with fever and cough. The chest radiography showed viral pneumonia and the nasopharyngeal swab detected SARS-CoV-2. He rapidly developed hypotension, oliguria and increased myocardial injury markers and was treated with adrenaline, antiviral drugs and mechanical ventilation. Echocardiography revealed diffuse myocardial hypo-akinesia and decreased left ventricular ejection fraction (LVEF). After several days of treatment, the patient was weaned off mechanical ventilation, LVEF recovered to 50% and laboratory tests showed a decrease of markers of myocardial injury. Coronavirus disease 2019 (COVID-19) can therefore severely affect myocardium with life-threatening complications and even young people can be involved.

7.
Eur Heart J Case Rep ; 5(2): ytaa518, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1010349

ABSTRACT

BACKGROUND: COVID-19 may induce a coagulation dysregulation resulting in a prothrombotic state with a higher risk of arterial and venous thrombosis. This abnormal thrombotic diathesis can lead to pulmonary embolism, stroke, and intracardiac thrombosis. CASE SUMMARY: We present two cases of unusual intracardiac thrombosis in patients hospitalized for COVID-19. In both cases, imaging tests (such as transthoracic echocardiography (TTE), computed tomography scan of the chest, and cardiac magnetic resonance imaging) showed evidence of unusual intracardiac thrombosis with thrombi adherent to regularly contracting walls. DISCUSSION: This evidence confirms that COVID-19 induces a hypercoagulable state which can result in intracardiac thrombosis. Therefore, TTE is indicated in all COVID-19 patients for early diagnosis, and prompt anticoagulant therapy is to be considered as a thromboprophylaxis strategy.

8.
JACC Case Rep ; 2(9): 1359-1364, 2020 Jul 15.
Article in English | MEDLINE | ID: covidwho-597754

ABSTRACT

Left ventricle thrombus is considered a rare complication of Takotsubo syndrome. However, both a stress condition predisposing to Takotsubo syndrome and coagulation abnormalities coexist in COVID-19. We describe a case of a patient with COVID-19 with Takotsubo syndrome. (Level of Difficulty: Intermediate.).

9.
JACC Case Rep ; 2(9): 1240-1244, 2020 Jul 15.
Article in English | MEDLINE | ID: covidwho-574717

ABSTRACT

A 34-year-old man was admitted with acute lung injury and COVID-19 pneumonia. In the intensive care unit, he experienced episodes of prolonged asystole accompanied by hypotension without loss of consciousness. Once reversible causes were excluded, symptoms were related to dysfunction of the sinus node, and the patient underwent implantation of a pacemaker. (Level of Difficulty: Beginner.).

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