High sensitive troponin I (hsTnI) is one of the markers of cardiac damage. Its values increase two to three hours after a heart attack and remain elevated for days. Recent studies have shown that kidneys are the main organ of elimination of troponin from blood. Our previous studies have shown that troponin I is removed and concentrated in the first morning urine. Increased blood pressure is one of the most common comorbidities today. By measuring blood pressure, we can see the current value of the pressure, but we do not know what the values are during the rest of the day. The aim of our research was to determine if there is a difference in the concentration of troponin I in urine among patients suffering from hypertension and among healthy individuals. The study involved 20 participants divided into two groups. In the first group were healthy individuals, while in the second group were individuals with hypertension. The first morning urine was sampled and the hsTnI was measured using a highsensitivity test on the Immuno-enzymatic analyser Abbott Architect i1000SR. Within the normotensive group, the mean value of hsTnI in the first morning urine was 14.95 pg/mL, while in the group of participants with elevated blood pressure, the mean value of hsTnI in the first morning urine was 26.59 pg/mL. The difference between these two groups was statistically significant with p=0.0451 (p<0.05). By measuring hsTnI in urine and determining the difference between healthy and those with hypertension, a new diagnostic test for hypertension monitoring and detection would be obtained.
<p><strong>Objective. </strong>Angioedema (AE) is a potentially life-threatening event. We investigated the etiology of AE, with the emphasis on bradykinininduced angioedema treatment in emergency medicine.</p><p><strong>Methods. </strong>The retrospective study included 237 patients with AE, who were examined and treated in two hospitals (group A and B) in Croatia from 2009 to 2016. The location and duration of AE, data about chronic diseases and treatment, potential causative agents (food, drugs, insect bites and chemicals), physical examination data and the subsequent treatment were analyzed.</p><p><strong>Results. </strong>There was no statistical difference regarding age or comorbidities but there was a statistically significant difference in etiology between the groups (Chi-square, P=0.03). Renin-angiotensin-aldosterone system (RAAS) blocker induced AE was the main cause of emergency attendance in group A (37.5%) and among the leading causes in group B (18.8%). Bradykinin-induced AE (hereditary angioedema (HAE) and RAAS-AE) were the leading causes in a total of 75 (31.5%) patients. RAAS-AE was treated with glucocorticoids and antihistamines. HAE attacks in both groups (2/7 patients, 1.5/6%) were treated with specific therapy. Other causes of AE in groups A/B were insect bites (15/23 patients, 13.5/20%), use of antibiotics/analgetics (11/17 patients, 9/15%), gastroesophageal reflux disease (10/11 patients, 8/9%), neoplasms (5/6 patients, 4/5%) and idiopatic (32/31 patients, 26.5/26%). 21% of patients were hospitalized.</p><p><strong>Conclusion. </strong>Bradykinin-mediated AE was the main cause of emergency attendance associated with AE. Advances in the treatment of HAE, with case reports of patients with RAAS-AE treated with C1 esterase inhibitor concentrate or bradykinin receptor antagonist, may prove to be a new, reliable and efficacious therapy option.</p>
Studies have documented independent contribution of sympathetic activation to the cardiovascular disease continuum. Hypertension is one of the leading modifiable factors. Most if not all the benefit of antihypertensive treatment depends on blood pressure lowering, regardless how it is obtained. Resistant hypertension is defined as blood pressure that remains uncontrolled in spite of the concurrent use of three antihypertensive drugs of different classes. Ideally, one of the three drugs should be a diuretic, and all drugs should be prescribed at optimal dose amounts. Poor adherence to antihypertensive therapy, undiscovered secondary causes (e.g. obstructive sleep apnea, primary aldosteronism, renal artery stenosis), and lifestyle factors (e.g. obesity, excessive sodium intake, heavy alcohol intake, various drug interactions) are the most common causes of resistant hypertension. Cardio(reno)vascular morbidity and mortality are significantly higher in resistant hypertensive than in general hypertensive population, as such patients are typically presented with a long-standing history of poorly controlled hypertension. Early diagnosis and treatment is needed to avoid further end-organ damage to prevent cardiorenovascular remodeling. Treatment strategy includes lifestyle changes, adding a mineralocorticoid receptor antagonist, treatment adherence in cardiovascular prevention and, in case of failure to control blood pressure, renal sympathetic denervation or baroreceptor activation therapy. The comparative outcomes in resistant hypertension deserve better understanding. In this review, the most current approaches to resistant hypertension and cardiovascular risk based on the available literature evidence will be discussed.
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