Case Report: Changes of Vascular Reactivity and Arterial Stiffness in a Patient With Covid-19 Infection.
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SUBMITTER: Jud P
PROVIDER: S-EPMC8149731 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundThe COVID-19 pandemic, caused by the Severe Acute Respiratory Syndrome Coronavirus 2 virus, emerged in late 2019 and spready globally. Many effects of infection with this pathogen are still unknown, with both chronic and repeated COVID-19 infection producing novel pathologies.Case presentationAn immunocompromised patient presented with chronic COVID-19 infection. The patient had history of Hodgkin's lymphoma, treated with chemotherapy and stem cell transplant. During the course of their treatment, eleven respiratory samples from the patient were analyzed by whole-genome sequencing followed by lineage identification. Whole-genome sequencing of the virus present in the patient over time revealed that the patient at various timepoints harboured three different lineages of the virus. The patient was initially infected with the B.1.1.176 lineage before coinfection with BA.1. When the patient was coinfected with both B.1.1.176 and BA.1, the viral populations were found in approximately equal proportions within the patient based on sequencing read abundance. Upon further sampling, the lineage present within the patient during the final two timepoints was found to be BA.2.9. The patient eventually developed respiratory failure and died.ConclusionsThis case study shows an example of the changes that can happen within an immunocompromised patient who is infected with COVID-19 multiple times. Furthermore, this case demonstrates how simultaneous coinfection with two lineages of COVID-19 can lead to unclear lineage assignment by standard methods, which are resolved by further investigation. When analyzing chronic COVID-19 infection and reinfection cases, care must be taken to properly identify the lineages of the virus present.
| S-EPMC10768205 | biostudies-literature
Project description:BackgroundCoronavirus disease 2019 (COVID-19) has spread rapidly worldwide since the outbreak originated in Wuhan, China in December 2019. Cardiovascular complications in patients with severe COVID-19 have been reported and are associated with a worse outcome. Coagulopathy is one of the most common life-threatening complication increasing mortality; however, little evidence is available regarding prevention strategies or its treatment in COVID-19 patients.Case summaryWe report a case of a 70-year-old woman admitted to hospital with severe COVID-19 bilateral pneumonia who developed severe coagulopathy with multiple both, venous and arterial, embolisms in major vessels such as bilateral pulmonary embolism, acute thrombus in abdominal aorta, and acute thrombotic occlusion of the right iliac common artery. The patient underwent emergent surgical thrombectomy of the right lower limb; in spite of anticoagulant treatment at therapeutic doses, patient presented poor clinical evolution and an infracondylar amputation of right lower limb was made finally. Subsequently, the patient received low molecular weight heparin (LMWH), antibiotics and antiviral therapy improving her renal function and her pneumonia, so she could be discharged safely.DiscussionProthrombotic coagulopathy due to enhanced acute inflammatory response and diffuse intravascular coagulation has been described in severe critical COVID-19 patients. This state of hypercoagulability is associated with organ dysfunction and mortality and may predispose to both, venous and arterial, thromboembolism. Little data are available regarding the best therapeutic and prevention strategies in this scenario, although thrombosis prophylaxis with LMWH has been associated with a better outcome.
| S-EPMC7717195 | biostudies-literature
Project description:Vascular calcification is a risk factor that predicts adverse cardiovascular complications of several diseases including atherosclerosis. Reduced dietary potassium intake has been linked to cardiovascular diseases such as hypertension and incidental stroke, although the underlying molecular mechanisms remain largely unknown. Using the ApoE-deficient mouse model, we demonstrated for the first time to our knowledge that reduced dietary potassium (0.3%) promoted atherosclerotic vascular calcification and increased aortic stiffness, compared with normal (0.7%) potassium-fed mice. In contrast, increased dietary potassium (2.1%) attenuated vascular calcification and aortic stiffness. Mechanistically, reduction in the potassium concentration to the lower limit of the physiological range increased intracellular calcium, which activated a cAMP response element-binding protein (CREB) signal that subsequently enhanced autophagy and promoted vascular smooth muscle cell (VSMC) calcification. Inhibition of calcium signals and knockdown of either CREB or ATG7, an autophagy regulator, attenuated VSMC calcification induced by low potassium. Consistently, elevated autophagy and CREB signaling were demonstrated in the calcified arteries from low potassium diet-fed mice as well as aortic arteries exposed to low potassium ex vivo. These studies established a potentially novel causative role of dietary potassium intake in regulating atherosclerotic vascular calcification and stiffness, and uncovered mechanisms that offer opportunities to develop therapeutic strategies to control vascular disease.
| S-EPMC5841863 | biostudies-literature
Project description:Several bone marrow-derived cell populations have been identified that may possess angiogenic activity and contribute to vascular homeostasis in experimental studies. We examined the extent to which lower quantities of these circulating angiogenic cell phenotypes may be related to impaired vascular function and greater arterial stiffness.We studied 1948 Framingham Heart Study participants (mean age, 66±9 years; 54% women) who were phenotyped for circulating angiogenic cells: CD34+, CD34+/KDR+, and early outgrowth colony forming units (CFU). Participants underwent non-invasive assessments of vascular function including peripheral arterial tone (PAT), arterial tonometry, and brachial reactivity testing.In unadjusted analyses, higher CD34+ and CD34+/KDR+ concentrations were modestly associated with lower PAT ratio (?=-0.052±0.011, P<0.001 and ?=-0.030±0.011, P=0.008, respectively) and with higher carotid-brachial pulse wave velocity (?=0.144±0.043, P=0.001 and ?=0.112±0.043, P=0.009), but not with flow-mediated dilation; higher CD34+ was also associated with lower carotid-femoral pulse wave velocity (?=-0.229±0.094, P=0.015). However, only the association of lower CD34+ concentration with higher PAT ratio persisted in multivariable analyses that adjusted for standard cardiovascular risk factors. In all analyses, CFU was not associated with measures of vascular function or arterial stiffness.In our large, community-based sample of men and women, circulating angiogenic cell phenotypes largely were not associated with measures of vascular function or arterial stiffness in analyses adjusting for traditional risk factors.
| S-EPMC3277804 | biostudies-literature
Project description:IntroductionThe spread of severe acute respiratory syndrome coronavirus 2 has resulted in coronavirus disease 2019 (COVID-19) pandemic, raising significant concerns. COVID-19 can lead to thrombotic complications such as acute limb ischemia (ALI). In patients with COVID-19, thrombotic complications may increase the risk of morbidity and mortality.Presentation of caseWe report the case of a 37-year-old man who presented with a 2 weeks history of right foot pain, toes blackish discoloration, and numbness. He tested positive for COVID-19 10 days prior to his presentation. Computed tomography angiography (CTA) of the lower limbs revealed near-complete occlusion of the right popliteal artery with single-vessel posterior tibial artery runoff. The patient was brought to a hybrid operating room, and diagnostic angiography confirmed the diagnosis. He underwent popliteal artery thromboembolectomy and intraoperative thrombolysis through a posterior approach. A completion angiography demonstrated a patent popliteal artery with a 2-vessels patency to the foot. His postoperative recovery was uneventful. After surgery, the popliteal, anterior tibial, and posterior tibial arteries were all palpable. The patient was discharged home on antiplatelet therapy with frequent postoperative follow-ups during the last 1 year in our outpatient clinic.DiscussionThe frequency of ALI has reduced worldwide, and the hypercoagulable condition remains an infrequent cause of limb ischemia. Patients with COVID-19 have a 35%-45% thromboembolic complication rate. In many studies, the virus launches a second attack between 7 and 14 days after symptom onset, possibly causing hypercoagulability. If conservative treatment fails, various surgical methods, including thromboembolectomy, thrombolysis, and thrombosuction, can be performed to treat ALI.ConclusionIn mild ALI symptoms, unfractionated heparin can be used with vigilant follow-up. Open and endovascular procedures are currently used to treat patients with acute limb ischemia, and technological advancements continue to make interventions easier and safer.
| S-EPMC9927001 | biostudies-literature
Project description:Endothelial dysfunction and vascular smooth muscle cell (VSMC) plasticity are critically involved in the pathogenesis of hypertension and arterial stiffness. MicroRNAs can mediate the cellular communication between vascular endothelial cells (ECs) and neighboring cells. Here, we investigated the role of endothelial-derived extracellular microRNA-92a (miR-92a) in promoting arterial stiffness by regulating EC-VSMC communication. Serum miR-92a level was higher in hypertensive patients than controls. Circulating miR-92a level was positively correlated with pulse wave velocity (PWV), systolic blood pressure (SBP), diastolic blood pressure (DBP), and serum endothelin-1 (ET-1) level, but inversely with serum nitric oxide (NO) level. In vitro, angiotensin II (Ang II)-increased miR-92a level in ECs mediated a contractile-to-synthetic phenotype change of co-cultured VSMCs. In Ang II-infused mice, locked nucleic acid-modified antisense miR-92a (LNA-miR-92a) ameliorated PWV, SBP, DBP, and impaired vasodilation induced by Ang II. LNA-miR-92a administration also reversed the increased levels of proliferative genes and decreased levels of contractile genes induced by Ang II in mouse aortas. Circulating serum miR-92a level and PWV were correlated in these mice. These findings indicate that EC miR-92a may be transported to VSMCs via extracellular vesicles to regulate phenotype changes of VSMCs, leading to arterial stiffness.
| S-EPMC8748448 | biostudies-literature
Project description:Background:Aldosterone is involved in almost all parts of the cardiovascular system. Hyperaldosteronism causes arterial hypertension and might predispose to stroke, atrial fibrillation, and heart failure. Case summary:A 60-year-old obese woman with long-standing hypertension, hypokalaemia, and shortness of breath was admitted to our hospital. Hypertension was caused by primary hyperaldosteronism due to an adenoma of the adrenal gland. Detailed transthoracic echocardiography revealed diastolic dysfunction, disturbed ventricular-arterial interaction, and atrial compliance resulting in heart failure with preserved ejection fraction (HFPEF). Three months of aldosterone antagonist treatment improved ventricular-arterial coupling, while left ventricular diastolic and atrial dysfunction remained unchanged. Discussion:Presumably, hyperaldosteronism is the reason for HFPEF in this case. Standard criteria to diagnose HFPEF include clinical symptoms of heart failure and an ejection fraction (EF) >50% as well as echocardiographically or invasively assessed elevated filling pressures. Single beat pressure-volume analysis gives insights on the pathophysiology of increased filling pressures, showing in our case diastolic dysfunction as well as disturbed ventricular-arterial interaction. Three months of aldosterone antagonist treatment reduced blood pressure with concomitant improvement of ventricular-arterial interaction, thereby reducing stroke work while stroke volume remained nearly unchanged. Diastolic dysfunction and increased atrial stiffness were unaltered.
| S-EPMC6939786 | biostudies-literature
Project description:BackgroundCardiovascular complications of COVID-19 have been reported in the adult population including myocarditis. However, less is known about the myocardial involvement in paediatric patients.Case summaryA 15-year-old boy was admitted to our intensive cardiac care unit with COVID-19 and an isolated acute myocarditis, confirmed on cardiac magnetic resonance imaging. No pulmonary lesion was observed on the chest CT scan. We report here the initial presentation, medical care, and clinical course of this patient.DiscussionIn the context of the acute COVID-19 outbreak, screening for COVID-19 infection should be performed in children presenting with myocardial injury in an inflammatory context.
| S-EPMC7528934 | biostudies-literature
Project description:We investigated intra-host genetic evolution using two SARS-CoV-2 isolates from a fully vaccinated (primary schedule x2 doses of AstraZeneca plus a booster of Pfizer), >70-year-old woman with a history of lymphoma and hypertension who presented a SARS-CoV-2 infection for 3 weeks prior to death due to COVID-19. Two full genome sequences were determined from samples taken 13 days apart with both belonging to Pango lineage FL.2: the first detection of this Omicron sub-variant in Botswana. FL.2 is a sub-lineage of XBB.1.9.1. The repertoire of mutations and minority variants in the Spike protein differed between the two time points. Notably, we also observed deletions within the ORF1a and Membrane proteins; both regions are associated with high T-cell epitope density. The internal milieu of immune-suppressed individuals may accelerate SARS-CoV-2 evolution; hence, close monitoring is warranted.
| S-EPMC10719116 | biostudies-literature
Project description:BackgroundArterial stiffness is an independent predictor of outcomes for patients with cardiovascular disease. Although measurement of pulse wave velocity is a widely accepted, noninvasive approach for the assessment of arterial stiffness, its accuracy is affected by changes in blood pressure.SummaryThe cardio-ankle vascular index (CAVI) is an index of the overall stiffness of the artery from the origin of the aorta to the ankle and is theoretically independent of blood pressure at the time of measurement. CAVI increases linearly with age and is elevated even in mild arteriosclerotic disease. It can identify differences in the degree of arteriosclerosis among patients with severe arteriosclerotic disease and better reflects the severity of disease of the coronary artery than does brachial-ankle pulse wave velocity. Patients with higher CAVI values show a poor prognosis compared with those with lower CAVI values. Furthermore, CAVI can be lowered by controlling diabetes mellitus and hypertension.Key messagesThe primary aims of assessing arterial stiffness using CAVI are to assist in the early detection of arteriosclerosis, allowing timely treatment and lifestyle modification, and to quantitatively evaluate the progression of disease and the effectiveness of treatment. Whether CAVI-guided therapy can improve prognosis in high-risk patients needs to be further examined to confirm the clinical usefulness of this measure.
| S-EPMC4949370 | biostudies-literature