Objective 

Hypertensive pulmonary edema is a fatal condition unless early and properly diagnosed and managed. Central blood pressure (cBP) has been proven to be more associated with adverse cardiovascular events. We aimed to study the correlation between cBP and heart damage in patients with Hypertensive pulmonary edema.

Methods 

We included 50 patients admitted to the emergency department in a university hospital for hypertensive pulmonary edema, 27 women and 23 men aged 50 to 70 years. We excluded patients with suspected acute coronary syndrome, significant valvular heart disease, and pericardial diseases. We measured cBP non-invasively from pulse wave analysis of the brachial artery. Brain natriuretic peptide (BNP) and cBP were repeatedly measured for every patient.

Results 

The median BNP levels of patients significantly decreased from 284 pg/ml (232–352.5) to 31.5 pg/ml (24–54) on discharge, P < 0.001. We found a significant correlation between admission BNP and central SBP (cSBP), urea, creatinine, arterial blood gases parameters, and left ventricular end-diastolic diameter (LVEDD). Concurrently, BNP at discharge was correlated with age, central DBP (cDBP), urea, creatinine, LVEDD, partial oxygen pressure (pO₂), and oxygen saturation (SO₂). Delta BNP was correlated with cSBP, peripheral SBP, urea, creatinine, pO₂, and SO₂. Linear regression analysis revealed that creatinine, and cSBP, were independent predictors of admission BNP, while urea and cDBP were the independent predictors of discharge BNP.

Conclusion 

This simple, noninvasive method of cBP measurement was significantly associated with the extent of myocardial damage in patients presenting with hypertensive pulmonary edema.

We aimed to determine the levels of follicular helper T (Tfh) and follicular regulatory T (Tfr) cells in COVID-19 patients and determine whether their levels correlated with disease severity and presence of hyperglycemia. This study was carried out in 34 hospitalized COVID-19 patients and 20 healthy controls. Levels of total circulating Tfh, inducible T-cell costimulator (ICOS)+ activated Tfh, and Tfr cells were assessed in all participants by flow cytometry. Total CD4+CXCR5+ Tfh cells and ICOS+Foxp3-activated Tfh cells increased and ICOS+Foxp3+ Tfr cells decreased in COVID-19 patients, especially in diabetic patients and those with severe disease. Activated ICOS+ Tfh cells were directly correlated with lactate dehydrogenase, D-dimer, ferritin, and respiratory rate and inversely correlated with the partial pressure of carbon dioxide. COVID-19 is associated with marked activation of Tfh cells and a profound drop in Tfr cells, especially in severe and diabetic patients. Future studies on expanded cohorts of patients are needed to clarify the relationship between SARS-CoV-2 and acute-onset diabetes.