Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 22
Filter
1.
Journal of Cardiovascular Development and Disease ; 9(1):15, 2022.
Article in English | MDPI | ID: covidwho-1613840

ABSTRACT

Background: It is uncertain whether exposure to renin–angiotensin system (RAS) modifiers affects the severity of the new coronavirus disease 2019 (COVID-19) because most of the available studies are retrospective. Methods: We tested the prognostic value of exposure to RAS modifiers (either angiotensin-converting enzyme inhibitors [ACE-Is] or angiotensin receptor blockers [ARBs]) in a prospective study of hypertensive patients with COVID-19. We analyzed data from 566 patients (mean age 75 years, 54% males, 162 ACE-Is users, and 147 ARBs users) hospitalized in five Italian hospitals. The study used systematic prospective data collection according to a pre-specified protocol. All-cause mortality during hospitalization was the primary outcome. Results: Sixty-six patients died during hospitalization. Exposure to RAS modifiers was associated with a significant reduction in the risk of in-hospital mortality when compared to other BP-lowering strategies (odds ratio [OR]: 0.54, 95% confidence interval [CI]: 0.32 to 0.90, p = 0.019). Exposure to ACE-Is was not significantly associated with a reduced risk of in-hospital mortality when compared with patients not treated with RAS modifiers (OR: 0.66, 95% CI: 0.36 to 1.20, p = 0.172). Conversely, ARBs users showed a 59% lower risk of death (OR: 0.41, 95% CI: 0.20 to 0.84, p = 0.016) even after allowance for several prognostic markers, including age, oxygen saturation, occurrence of severe hypotension during hospitalization, and lymphocyte count (adjusted OR: 0.37, 95% CI: 0.17 to 0.80, p = 0.012). The discontinuation of RAS modifiers during hospitalization did not exert a significant effect (p = 0.515). Conclusions: This prospective study indicates that exposure to ARBs reduces mortality in hospitalized patients with COVID-19.

2.
European heart journal supplements : journal of the European Society of Cardiology ; 23(Suppl G), 2021.
Article in English | EuropePMC | ID: covidwho-1602236

ABSTRACT

Aims Although the new coronavirus (SARS-CoV-2) may cause an acute multiorgan syndrome (COVID-19), data are emerging on mid- and long-term sequelae of COVID-19 pneumonia. Since no study has hitherto investigated the role of both cardiac and pulmonary ultrasound techniques in detecting such sequelae, this study aimed at evaluating these simple diagnostic tools to appraise the cardiopulmonary involvement occurring after COVID-19 pneumonia. Methods and results Twenty-nine patients fully recovered from COVID-19 pneumonia were considered at our centre. On admission, all patients underwent 12-lead electrocardiogram (ECG) and transthoracic echocardiography (TTE) evaluation. Compression ultrasound (CUS) and lung ultrasound (LUS) were also performed. Finally, in each patient, pathological findings detected on LUS were correlated with the pulmonary involvement occurring after COVID-19 pneumonia as assessed on thoracic computed tomography (CT). Out of 29 patients (mean age 70 ± 10 years old;M 69%), prior cardiovascular and pulmonary comorbidities were recorded in 22 (76%). Twenty-seven patients (93%) were in sinus rhythm and two (7%) in atrial fibrillation. ECG repolarization abnormalities were extremely common (93%) and reflected the high prevalence of pericardial involvement on TTE (86%). Likewise, pleural abnormalities were frequently observed (66%). TTE signs of left and right ventricular dysfunction were reported in two patients only, but values of systolic pulmonary artery pressure were abnormal in 16 (55%) despite absence of prior comorbidities in 44% of them. Regarding LUS evaluation, most patients displayed abnormal values of diaphragmatic thickness and excursion (93%) which well correlated with the high prevalence (76%) of on pathological findings on CT scan. CUS ruled out deep vein thrombosis in all patients. Conclusions Data on cardiopulmonary sequelae after COVID-19 pneumonia are scarce. In our study, simple diagnostic tools (TTE and LUS) proved clinically useful for detection of cardiopulmonary involvement after COVID-19 pneumonia.

3.
European heart journal supplements : journal of the European Society of Cardiology ; 23(Suppl G), 2021.
Article in English | EuropePMC | ID: covidwho-1602008

ABSTRACT

Aims Myopericarditis have been reported as rare event after SARS-CoV-2 vaccination with mRNA-1273 and BNT162b2. However, these data referred to the month of May 2021, when only a few people under the age of 30 had been vaccinated. The aim was to report cases diagnosed with myopericarditis short after vaccination admitted to our hospital. Methods and results An observational study was performed recording all cases of patients (pts) hospitalized for myopericarditis which occurred within 14 days of SARS-CoV-2 mRNA vaccination. From June to August 2021, 12 pts were hospitalized for myopericarditis;four of them (33%) were young male pts (29 ± 12 years old) with no history of CVDs or SARS-CoV-2 infection but with a recent second dose of Covid-19 mRNA-1273 vaccine (mean interval from the injection 3 ± 2 days). ECG showed diffuse ST-segment elevation without specularity (Figure 1). SARS-CoV-2 molecular swab tested negative;laboratory (lab) test showed a slight increase of white blood cells (11 267 ± 1047 108/l) and a marked increase of C-reactive protein (78 ± 79 mg/l), troponin T (179 ± 179 ng/l), and Nt-proBNP (876 ± 198 ng/l);transthoracic echocardiogram showed normal left ventricle ejection fraction (mean 55 ± 3%) and in one case only mild pericardial effusion;chest X-ray showed pleural effusion in one case only. Pts were then hospitalized for an average of 7 ± 2 days and an anti-inflammatory therapy based on acetylsalicylic acid and colchicine (in one case also with cortisone) was established. In the following days, pts gradually recovered and were discharged home. After 10 days, two pts underwent a cardiac magnetic resonance imaging (cMRI) revealing myocardial oedema and late gadolinium enhancement in the subepicardial and midmyocardium, along the basal and mid-apical lateral wall;due to relative contraindications, the same examination was scheduled later for the other two pts. These cases deserve specific considerations on the causal relationship between heart inflammation and SARS-CoV-2 mRNA vaccines. Among the various pathophysiological hypothesis there is the high levels of antibodies that mRNA vaccines can generate in young male subjects or the consideration of mRNA as a natural adjuvant capable of activating disproportionately the innate immune system;in both cases, the result is an immune overreaction that can affect various organs including the heart. Conclusions Although the number of our cases is small and all pts recovered in a short time, the timing of symptoms and the similarities in clinical findings and lab characteristics call for further investigations.

4.
European heart journal supplements : journal of the European Society of Cardiology ; 23(Suppl G), 2021.
Article in English | EuropePMC | ID: covidwho-1602007

ABSTRACT

Aims Severe pulmonary complications are well described in the coronavirus disease 2019 (COVID-19) and cardiovascular diseases (CVDs) have been documented as well. Most patients (pts) recover quickly;nevertheless, the potential long-term cardiovascular sequalae of COVID-19 remain currently unknown. The aim was to report cases of acute coronary syndromes (ACS) after healing from COVID-19 and their features at coronary angiography;secondary purpose was to hypothesize the underlying mechanisms. Methods and results A retrospective study was performed by acquiring data from the electronic medical record. From January to June 2021, four hypertensive pts (64 ± 17 years old;three males) with no history of CVDs and previous symptomatic SARS-CoV-2 infection (mean interval from first positive molecular swab 47 ± 32 days;all recovered after 15 days with double negative swab) were admitted to the emergency department for ST-elevation myocardial infarction (3 anterior and one inferior). At admission, the SARS-CoV-2 molecular swab tested negative, left ventricle ejection fraction was 42 ± 12%, troponin T and Nt-proBNP values were 47 ± 24 ng/l and 1180 ± 978 ng/l, respectively. Emergency coronary angiography showed single-vessel acute thrombotic occlusion (in three cases of the anterior descending artery and in one case of the right coronary artery), with no evidence of atherosclerotic disease. Because of the high thrombotic burden, in all cases a mechanical thrombus aspiration system was used, tirofiban infusion started and no balloon angioplasty or drug-eluting stent implantation was necessary (Figures A–D). After 72 h, a second SARS-CoV-2 molecular swab tested also negative. In the following days, the pts gradually recovered and they were discharged home. Conclusions These cases deserve specific considerations both on the pathophysiologic mechanisms of the ACS possibly related to SARS-CoV-2 and on the subsequent long-term sequelae. Among various pathophysiologic mechanisms proposed, the high affinity of the spike protein for the angiotensin converting enzyme two receptor (expressed by both cardiac and endothelial cells) could explain direct cardiac viral infection and vasculitis with possible development of thrombosis. The latter could contribute both to acute and long-term cardiac sequelae, even months after the acute infection, configuring a sort of ‘cardiac post-Covid syndrome’. Whether and how long this status persists, making COVID-19 a risk factor for subsequent CVDs, is still an unresolved question. In this regard, continuous monitoring of these pts and larger future studies will be essential.

5.
G Ital Cardiol (Rome) ; 23(1): 10-14, 2022 Jan.
Article in Italian | MEDLINE | ID: covidwho-1609112

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) rapidly spread across the world, killing more than 4 million individuals globally, with 240 million individuals being confirmed by laboratory tests. Among different therapeutic strategies to prevent SARS-CoV-2 infection, vaccines are the most promising approach for curbing the pandemic. They elicit an immune neutralizing response and thus offer protection against coronavirus disease 2019 (COVID-19). However, some questions regarding the safety of COVID-19 vaccines have been raised and based on sparse reports of severe systemic reactions after vaccination. Among these, evidences on the potential effect of vaccination on the acute rise in blood pressure have been recently accrued. Approved vaccines in Europe increase the endogenous synthesis of SARS-CoV-2 Spike proteins from a variety of cells. Once synthetized in the cells reached by the vaccine, the Spike proteins first assemble in the cytoplasm and then migrate to the cell surface to protrude with a native-like conformation. Spike proteins are recognized by the immune system which rapidly develops an immune response. Furthermore, the Spike proteins assembled in the cells which are eventually destroyed by the immune response circulate in the blood as free-floating forms. Free-floating Spike proteins may interact with angiotensin-converting enzyme 2 (ACE2) receptors leading to internalization, degradation, and dysregulation of the catalytic activities of these receptors. The consequent loss of ACE2 receptor activity leads to a rapid drop in the generation of angiotensin1,7 resulting from inactivation of angiotensin II. The imbalance between angiotensin II (overactivity) and of angiotensin1,7 (deficiency) might play a role in the genesis of acute elevation in blood pressure.


Subject(s)
COVID-19 , Hypertension , COVID-19 Vaccines , Humans , SARS-CoV-2 , Vaccination
6.
J Cardiovasc Dev Dis ; 8(10)2021 Oct 17.
Article in English | MEDLINE | ID: covidwho-1470897

ABSTRACT

BACKGROUND: Although severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) may cause an acute multiorgan syndrome (coronavirus disease 2019 (COVID-19)), data are emerging on mid- and long-term sequelae of COVID-19 pneumonia. Since no study has hitherto investigated the role of both cardiac and pulmonary ultrasound techniques in detecting such sequelae, this study aimed at evaluating these simple diagnostic tools to appraise the cardiopulmonary involvement after COVID-19 pneumonia. METHODS: Twenty-nine patients fully recovered from COVID-19 pneumonia were considered at our centre. On admission, all patients underwent 12-lead electrocardiogram (ECG) and transthoracic echocardiography (TTE) evaluation. Compression ultrasound (CUS) and lung ultrasound (LUS) were also performed. Finally, in each patient, pathological findings detected on LUS were correlated with the pulmonary involvement occurring after COVID-19 pneumonia, as assessed on thoracic computed tomography (CT). RESULTS: Out of 29 patients (mean age 70 ± 10 years; males 69%), prior cardiovascular and pulmonary comorbidities were recorded in 22 (76%). Twenty-seven patients (93%) were in sinus rhythm and two (7%) in atrial fibrillation. Persistence of ECG abnormalities from the acute phase was common, and nonspecific repolarisation abnormalities (93%) reflected the high prevalence of pericardial involvement on TTE (86%). Likewise, pleural abnormalities were frequently observed (66%). TTE signs of left and right ventricular dysfunction were reported in two patients, and values of systolic pulmonary artery pressure were abnormal in 16 (55%, despite the absence of prior comorbidities in 44% of them). Regarding LUS evaluation, most patients displayed abnormal values of diaphragmatic thickness and excursion (93%), which correlated well with the high prevalence (76%) of pathological findings on CT scan. CUS ruled out deep vein thrombosis in all patients. CONCLUSIONS: Data on cardiopulmonary involvement after COVID-19 pneumonia are scarce. In our study, simple diagnostic tools (TTE and LUS) proved clinically useful for the detection of cardiopulmonary complications after COVID-19 pneumonia.

8.
Expert Opin Pharmacother ; : 1-8, 2021 Oct 20.
Article in English | MEDLINE | ID: covidwho-1462202

ABSTRACT

INTRODUCTION: Hypertension is a common chronic disorder in patients hospitalized for coronavirus disease 2019 (COVID-19). Furthermore, an exaggerated cardiovascular response with persistently raised blood pressure during hospitalization seems independently associated with in-hospital all-cause mortality, intensive care unit admission and heart failure. However, the real burden of elevated blood pressure during the acute phase of COVID-19 remains undefined. AREAS COVERED: The authors review the available evidence on the pharmacotherapy for the treatment of acute elevations in blood pressure (including hypertensive urgency and emergency) in COVID-19 patients. EXPERT OPINION: Acute elevations in blood pressure and unstable in-hospital blood pressure may be associated with organ damage and worse outcome in patients with COVID-19. In this setting, hypertensive emergencies require immediate reduction in blood pressure through intravenous treatment according to specific features and goals. Conversely, hypertensive urgencies usually require solely oral treatment. Diuretics, beta-blockers, renin-angiotensin-aldosterone system inhibitors, and calcium channel blockers may be of benefit in treating COVID-19 patients with elevated blood pressure values.

10.
J Hypertens ; 39(8): 1555-1558, 2021 08 01.
Article in English | MEDLINE | ID: covidwho-1288136
12.
Clin Chem Lab Med ; 59(10): 1607-1609, 2021 06 14.
Article in English | MEDLINE | ID: covidwho-1266565
13.
Eur J Intern Med ; 88: 1-8, 2021 06.
Article in English | MEDLINE | ID: covidwho-1220830

ABSTRACT

Vaccines to prevent acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection elicit an immune neutralizing response. Some concerns have been raised regarding the safety of SARS-CoV-2 vaccines, largely based on case-reports of serious thromboembolic events after vaccination. Some mechanisms have been suggested which might explain the adverse cardiovascular reactions to SARS-CoV-2 vaccines. Different vaccine platforms are currently available which include live attenuated vaccines, inactivated vaccines, recombinant protein vaccines, vector vaccines, DNA vaccines and RNA vaccines. Vaccines increase the endogenous synthesis of SARS-CoV-2 Spike proteins from a variety of cells. Once synthetized, the Spike proteins assembled in the cytoplasma migrate to the cell surface and protrude with a native-like conformation. These proteins are recognized by the immune system which rapidly develops an immune response. Such response appears to be quite vigorous in the presence of DNA vaccines which encode viral vectors, as well as in subjects who are immunized because of previous exposure to SARS-CoV-2. The resulting pathological features may resemble those of active coronavirus disease. The free-floating Spike proteins synthetized by cells targeted by vaccine and destroyed by the immune response circulate in the blood and systematically interact with angiotensin converting enzyme 2 (ACE2) receptors expressed by a variety of cells including platelets, thereby promoting ACE2 internalization and degradation. These reactions may ultimately lead to platelet aggregation, thrombosis and inflammation mediated by several mechanisms including platelet ACE2 receptors. Whereas Phase III vaccine trials generally excluded participants with previous immunization, vaccination of huge populations in the real life will inevitably include individuals with preexisting immunity. This might lead to excessively enhanced inflammatory and thrombotic reactions in occasional subjects. Further research is urgently needed in this area.


Subject(s)
COVID-19 , Thrombosis , COVID-19 Vaccines , Humans , SARS-CoV-2
14.
Eur J Intern Med ; 89: 81-86, 2021 07.
Article in English | MEDLINE | ID: covidwho-1209445

ABSTRACT

AIMS: heart failure (HF) and coronary artery disease (CAD) are independent predictors of death in patients with COVID-19. The adverse prognostic impact of the combination of HF and CAD in these patients is unclear. METHODS AND RESULTS: we analysed data from 954 consecutive patients hospitalized for SARS-CoV-2 in five Italian Hospitals from February 23 to May 22, 2020. The study was a systematic prospective data collection according to a pre-specified protocol. All-cause mortality during hospitalization was the outcome measure. Mean duration of hospitalization was 33 days. Mortality was 11% in the total population and 7.4% in the group without evidence of HF or CAD (reference group). Mortality was 11.6% in the group with CAD and without HF (odds ratio [OR]: 1.6, p = 0.120), 15.5% in the group with HF and without CAD (OR: 2.3, p = 0.032), and 35.6% in the group with CAD and HF (OR: 6.9, p<0.0001). The risk of mortality in patients with CAD and HF combined was consistently higher than the sum of risks related to either disorder, resulting in a significant synergistic effect (p<0.0001) of the two conditions. Age-adjusted attributable proportion due to interaction was 64%. Adjusting for the simultaneous effects of age, hypotension, and lymphocyte count did not significantly lower attributable proportion which persisted statistically significant (p = 0.0360). CONCLUSION: The combination of HF and CAD exerts a marked detrimental impact on the risk of mortality in hospitalized patients with COVID-19, which is independent on other adverse prognostic markers.


Subject(s)
COVID-19 , Coronary Artery Disease , Heart Failure , Hospitalization , Humans , Italy/epidemiology , Prospective Studies , Risk Factors , SARS-CoV-2
15.
17.
Eur J Intern Med ; 78: 101-106, 2020 08.
Article in English | MEDLINE | ID: covidwho-609614

ABSTRACT

BACKGROUND: . The electrocardiographic (ECG) changes which may occur during hospitalization for COVID-19 have not yet been comprehensively assessed. PATIENTS AND METHODS: . We examined 50 patients admitted to hospital with proven COVID-19 pneumonia. At entry, all patients underwent a detailed clinical examination, 12-lead ECG, laboratory tests and arterial blood gas test. ECG was also recorded at discharge and in case of worsening clinical conditions. RESULTS: . Mean age of patients was 64 years and 72% were men. At baseline, 30% of patients had ST-T abnormalities, and 33% had left ventricular hypertrophy. During hospitalization, 26% of patients developed new ECG abnormalities which included atrial fibrillation, ST-T changes, tachy-brady syndrome, and changes consistent with acute pericarditis. One patient was transferred to intensive care unit for massive pulmonary embolism with right bundle branch block, and another for non-ST segment elevation myocardial infarction. Patients free of ECG changes during hospitalization were more likely to be treated with antiretrovirals (68% vs 15%, p = 0.001) and hydroxychloroquine (89% vs 62%, p = 0.026) versus those who developed ECG abnormalities after admission. Most measurable ECG features at discharge did not show significant changes from baseline (all p>0.05) except for a slightly decrease in Cornell voltages (13±6 vs 11±5 mm; p = 0.0001) and a modest increase in the PR interval. The majority (54%) of patients with ECG abnormalities had 2 prior consecutive negative nasopharyngeal swabs. ECG abnormalities were first detected after an average of about 30 days from symptoms' onset (range 12-51 days). CONCLUSIONS: . ECG abnormalities during hospitalization for COVID-19 pneumonia reflect a wide spectrum of cardiovascular complications, exhibit a late onset, do not progress in parallel with pulmonary abnormalities and may occur after negative nasopharyngeal swabs.


Subject(s)
Arrhythmias, Cardiac , Coronavirus Infections , Electrocardiography/methods , Pandemics , Pneumonia, Viral , Arrhythmias, Cardiac/classification , Arrhythmias, Cardiac/diagnosis , Arrhythmias, Cardiac/etiology , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/diagnosis , Coronavirus Infections/epidemiology , Coronavirus Infections/physiopathology , Coronavirus Infections/therapy , Female , Hospitalization/statistics & numerical data , Humans , Italy/epidemiology , Male , Middle Aged , Outcome and Process Assessment, Health Care , Pneumonia, Viral/diagnosis , Pneumonia, Viral/epidemiology , Pneumonia, Viral/etiology , Pneumonia, Viral/physiopathology , Pneumonia, Viral/therapy , Prognosis , SARS-CoV-2 , Severity of Illness Index
18.
Hypertension ; 76(2): 294-299, 2020 08.
Article in English | MEDLINE | ID: covidwho-457026

ABSTRACT

Diffuse pulmonary inflammation, endothelial inflammation, and enhanced thrombosis are cardinal features of coronavirus disease 2019 (COVID-19), the disease caused by the severe acute respiratory syndrome coronavirus 2. These features are reminiscent of several adverse reactions triggered by angiotensin II and opposed by angiotensin1-7, in many experimental models. Severe acute respiratory syndrome coronavirus 2 binds to ACE2 (angiotensin-converting enzyme 2) receptors and entries into the cell through the fusion of its membrane with that of the cell. Hence, it downregulates these receptors. The loss of ACE2 receptor activity from the external site of the membrane will lead to less angiotensin II inactivation and less generation of antiotensin1-7. In various experimental models of lung injury, the imbalance between angiotensin II overactivity and of antiotensin1-7 deficiency triggered inflammation, thrombosis, and other adverse reactions. In COVID-19, such imbalance could play an important role in influencing the clinical picture and outcome of the disease. According to this line of thinking, some therapeutic approaches including recombinant ACE2, exogenous angiotensin1-7, and angiotensin receptor blockers seem particularly promising and are being actively tested.


Subject(s)
Angiotensin Receptor Antagonists/therapeutic use , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Betacoronavirus , Coronavirus Infections/drug therapy , Pneumonia, Viral/drug therapy , Renin-Angiotensin System/drug effects , COVID-19 , Coronavirus Infections/epidemiology , Coronavirus Infections/metabolism , Humans , Pandemics , Pneumonia, Viral/epidemiology , Pneumonia, Viral/metabolism , SARS-CoV-2
19.
Monaldi Arch Chest Dis ; 90(2)2020 May 20.
Article in English | MEDLINE | ID: covidwho-324649

ABSTRACT

The novel respiratory Syndrome Coronavirus-2 (SARS-CoV-2) caused a cluster of pneumonia cases in China at the end of 2019. After few months, it led to a pandemic that has spread throughout most countries of the world (https://coronavirus.jhu.edu/map.html).


Subject(s)
Coronavirus Infections , Hypertension , Pandemics , Pneumonia, Viral , Betacoronavirus , COVID-19 , Coronavirus Infections/complications , Humans , Hypertension/complications , Pneumonia, Viral/complications , SARS-CoV-2 , Severity of Illness Index
SELECTION OF CITATIONS
SEARCH DETAIL
...