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Hypertension and nephrology

SEPTEMBER 30, 2020

[Post-career development of cardiometabolic changes and hypertension in competitive athletes]


[Regular physical activity is essential in delaying the aging processes (e.g. arterial remodelling – stiffening, metabolism, bodyweight), the beneficial effects of competitive sports – especially strength sports – according to the recent data of the literature are questionable. The beneficial effects of physical activity on the cardiovascular (CV) system are well known, however less is known regarding the delayed impacts of high intensity competitive sports on the CV system, especially after the sport career is over. This review summarizes the effects of active competitive sport and the post-career period on the cardiometabolic system with special attention to the systemic blood pressure and the development of metabolic syndrome. After sport career, the welldeveloped high performance cardiovascular- and metabolic system suddenly is much less used, but still supported by sport-level diet. It is well known that hypertension is a significant pathogenic factor in the development of cardiovascular diseases, characterized – among others – by reduced elasticity of large- and medium- sized vessels thereby importantly contributing to the development of systolic hypertension. Inflammation and thrombus formation both play an important role in the development of vascular injury and atherosclerosis. The increased tone of microvessels can impair the blood supply of certain organs, including the coronary circulation. It has been ample shown, that regular non-competitive, aerobic exercise activities are important factors in preventing hypertension. Such pathological changes become more evident after the development of post-career obesity, as well as the development of hypertension due to the activation of the renin-angiotensin system through sodium retention and other metabolic changes (increased glucose tolerance, insulin resistance, type II diabetes mellitus). It has been ample shown, that regular non-competitive, dynamic aerobic exercise activities are important factors in preventing hypertension. The frequency, intensity, type, and time (FITT) principle of exercise prescription is the first and common therapeutic approach, which represents the translation of cardiovascular basic science research results into hypertension treatment, thus can provide a personalized physical activity program/therapy according to medical needs not just for the post-career sportspersons, but the wide range of patients.]

Clinical Neuroscience

JANUARY 30, 2020

[Current questions of multiple sclerosis: the secunder progressive form of the disease]


[Recent data suggest that long-term worsening is common in relapsing-remitting multiple sclerosis patients and is largely independent of relapses or new lesion formation on brain MRI. The current definition of secunder progressive multiple sclerosis is worsening of disability independent of relapses over at least 6-month interval. Early focal inflammatory disease activity and spinal cord lesion are predictors of very-long term disease outcomes in relapse - onset multiple sclerosis. The potential of PET imaging to visualize hidden inflammation in MS brain in vivo is an important contribution for better understanding the progression of the disease. Therefore, PET imaging is a promising tool in detecting the conversion from relapsing remitting multiple sclerosis to secunder progressive form of multiple sclerosis. Furthermore, neuro-axonal damage is the pathological substrate of permanent disability in different neurological disorders including multiple sclerosis. The neurofilament proteins have promise in this context because their levels rise upon neuro-axonal damage not only in the cerebrospinal fluid but also in blood. Patients with increased serum levels of neurofilament at baseline, independent of other clinical and MRI variables, experience significantly more brain and spinal cord volume loss over 2 years and 5 years of follow-up. The kynurenine-pathway abnormalities may be associated with the swich from early-mild stage multiple sclerosis to debilitating progressive forms of the disease. Analysis of these metabolites in serum may have application as multiple sclerosis disease biomarkers. Free radical action has been suggested as a causal factor in the illness. Increased free radical production and consumption of the scavenger molecules were found during the active phase of the disease. Based on the clinical findings (EXPAND Study) and pathomechanism of the disease siponimod is approved by the US Food and Drug Administration for the treatment of relapsing remitting forms of multiple sclerosis, to include secunder progressive multiple sclerosis with active disease, relapsing-remitting multiple sclerosis and clinically isolated syndrome.]

Lege Artis Medicinae

NOVEMBER 15, 2019

[The hypertensive, non-diabetic nephropathy]


[According to the increase of the number of the hypertensive patients the prevalence of hypertensive nephropathy will increase also. According to the data in the Registry of Hungarian Society of Hypertension, in 2015 the proportion of hypertension patients with chronic kidney disease was 12.3% of the males, 39.1% of the females and generally 26.1% of all the hypertensives. In Hungary the hypertensive nephropathy was the 2nd most common condition led to chronic dialysis in 2010 and 2015 (21% and 22%). According to the Hungarian Society of Hypertension 2018 Guideline the classic inhibitors of the renin-angiotensin system can decrease significantly the progression of renal function decline and the proteinuria. ]

Hypertension and nephrology

OCTOBER 23, 2019

[Blood pressure management for stroke prevention and in the acute stroke. The new guideline of European Society of Hypertension (ESH, 2018), European Society of Cardiology and Hungarian Society of Hypertension (HSH, 2018)]

JENEI Zoltán

[Hypertension is the leading modifiable risk factor for stroke. Its prevalence amongst stroke patient is about 60-70% and the benefit of blood pressure (BP) lowering therapy on stroke risk reduction is well established. However the optimal BP targets for preventing stroke and reducing stroke consequences have been controversial. The new European (ESC/ESH) and Hungarian (HSH) hypertension guideline published in 2018 highlighted the primary and secondary prevention of stroke and the BP management in the acute stroke care as well. According results from ACCORD, SPRINT, HOPE-3, and other metaanalysis the systolic blood pressure (SBP) lowering < 120 mmHg has not favourable effect, thus in hypertensive patients < 65 years the SBP should be lowered to a BP range of 120-129 mmHg. In older patients ≥ 65 years the SBP should be targeted to a BP range of 130-139 mmHg (IA). In patients with acute intracerebral haemorrhage careful acute BP lowering with iv. therapy, to <180 mmHg should be considered only in case of SBP ≥ 220 mmHg (IIaB). In patients with acute ischaemic stroke who are eligible for iv. thrombolysis, BP should be carefully lowered and maintained to < 180/105 mmHg for at least the first 24 h after thrombolysis (IIaB). If the patient is not eli gible for lysis and BP ≤ 220/110 mmHg, routine BP lowering drug therapy is not recommended inside 48-72 h (IA). In patients with markedly elevated BP > 220/110 mmHg who do not receive fibrinolysis, drug therapy may be considered, based on clinical judgement, to reduce BP by 15% during the first 24 h after the stroke onset (IIbC). After 72 h of acute stroke in case of hypertensive patients < 65 years the SBP should be lowered to a BP range of 120-129 mmHg (IIaB). In older patients ≥ 65 years the SBP should be targeted to a BP range of 130-139 mmHg (IA). If BP < 140/90 mmHg after stroke, the BP lowering should be considered (IIbA). It is recommended to initiate an antihypertensive treatment with combination, preferably single pill combination of renin-angiotensin system blockers plus a calcium channel blocker and/or a thiazide like diuretics (IA). Lowering SBP < 120 mmHg is not recommended due to advers events regardless of age and type of stroke either in primary or secondary stroke prevention.]

Hypertension and nephrology

MAY 10, 2019

[One-year persistence of fixed-dose combinations of angiotensin-converting enzyme inhibitor and calcium channel blocker in hypertensive patients]


[Introduction: The most recent European guidelines for the treatment of hypertension suggest the use of renin-angiotensin-aldosterone system antagonists (RAAS inhibitors) and calcium channel blockers (CCBs) or diuretics fixed-dose combinations (FDCs) as the first therapeutic option. In antihypertensive therapy, the patient’s adherence is one of the most important factors in reducing unwanted cardiovascular events. Aim: Our aim was to assess the one-year persistence of angiotensin-converting enzyme inhibitor (ACEI) and CCB FDCs in hypertensive patients. Method: Authors have analysed the prescription database of the National Health Insurance Fund in Hungary on pharmacy claims between October 1, 2012 and September 30, 2013. Those patients were identified who filled prescriptions for FDCs of ACEI and CCBs prescribed for the first time for hypertensive patients and who had not re ceived similar drugs during the year before. Apparatus of survival analysis was used, where ‘survival’ was the time to abandon the medication. Results: 124,388 patients met the inclusion criteria. One-year persistence rate and hazard ratio (HR) of discontinua tion in patients with ramipril/amlodipine FDC was 54% (HR = 1.00, reference), perindopril/amlodipine 47% (HR = 1.30, p<0.0001), lisinopril/amlodipine 36% (HR = 1.79, p<0.0001), ramipril/felodipine 26% (HR = 2.28, p<0.0001) and trandolapril/verapamil 12% (HR = 4.13, p<0.0001). The average survival time of drug limited to 360 days was 270.2 days for ramipril/amlodipine FDC, 242.7 days for perindopril/amlodipine FDC, 211.2 days for lisinopril/amlodipine FDC, 186.3 days for ramipril/felodipine FDC and 125.7 days for trandolapril/verapamil FDC. Conclusions: The authors demonstrated that the one-year persistence of ACEI/CCB FDCs was significantly different in hypertensive patients. Ramipril/amlodipine FDC was more advantageous for patient adherence.]

Hypertension and nephrology

SEPTEMBER 12, 2018

[Treatment of hypertension in kidney transplant patients]


[Most of the renal transplant recipients suffer from hypertension. Hypertension substantially contributes to the high cardiovascular mortality in this population. The recommendation of the Hungarian Society of Hypertension and the international guidelines suggest to achieve less than 130/80 mmHg as target blood pressure in these patients. Several factors may be in the background of hypertension after kidney transplantation, which can be summarized as factors from the recipient-side, the donorside and factors provoked by transplantation itself. In most of the cases early after transplantation high doses of immunosuppressive drugs (especially calcineurin inhibitors and steroids) are responsible for the increased blood pressure. There are some further special methods apart from the general recommendations which are needed during the examination of hypertension of kidney transplant patients: e.g. measurement of blood trough-level of immunosuppressive drugs, investigation of bone-mineral disorder, screening for the level and causes of anaemia, check-up of the renal graft circulation. Kidney transplant patients suffering from hypertension usually need more than two antihypertensive drugs beyond the use of non-pharmaceutical antihypertensive methods. In the early posttransplantation period calcium channel blockers are preferred antihypertensive medications, because they counterbalance the vasoconstrictive effect of calcineurin inhibitors. The administration of renin-angiotensin-aldosterone inhibitors are rather suggested after the stabilization of renal function (from the 1-3 months posttransplantation). When designing antihypertensive strategy, comorbidities and special factors should be regarded as well, especially volume overload, proteinuria, allograft function (GFR), diabetes, other cardiovascular risk factors, previous cardiovascular events. The setup of an individual therapeutical strategy is advised in view of all these factors, which is different according to the timing after transplantation: the perioperative, the early postoperative phases and from 1-3 months after transplantation have special focuses.]

Hypertension and nephrology

FEBRUARY 20, 2018

[How the recognition and treatment of primary aldosteronism could be improved?]


[Practically there were no randomized, controlled trials in the area of PA so far, but recently two such ones have appeared. In addition, both are paradigm- forming; yet not built into (yet?) the expert opinions. In the field of primary aldosteronism (PA), there is a sharp contrast between the world’s leading experts in many areas. There is consensus in respect that hypokalaemia, therapy resistance and vascular complications are more common in PA than in primary hypertension. According to prestigious studies, the ratio of surgically correctable cases can be around 5% of hypertension. However, only a tiny fraction of these cases are ever investigated even in the developed countries. Specific treatment might be reached more easily by a multi-speed approach applicable for domestic conditions in which one of the alternatives is the diagnostic process itself. In the latter, following aldosterone criteria are proposed: at screening greater than 15 ng/dl when associated with low renin, in the suppression test, for further testing (adrenal CT) a concentration above 5 ng/dl. This would provide a sufficient balance between sensitivity and specificity. Another solution could be the more widespread use of low dose spironolactone in resistant hypertension.]

Hypertension and nephrology

DECEMBER 20, 2016

[Hypertension and atrial fibrillation]

SZŐKE Vince Bertalan, BARACSI-BOTOS Viktória, JÁRAI Zoltán

[Hypertension is the most important independent risk factor of atrial fibrillation, the most common clinically significant arrhythmia. Increased atrial wall tension, myocardium remodelling, activation of renin-angiotensin-aldosterone system (RAAS) and fibrotic remodelling are possible hypertension induced mechanisms which can contribute to developing atrial fibrillation. Knowing the relation of hypertension to atrial fibrillation is crucial in the need for effective and up-to-date therapeutic strategies. RAAS inhibitors and beta blockers prevent atrial fibrillation not only by lowering blood pressure but partly due to the inhibition of the above mentioned mechanisms. Complications of hypertension, such as left ventricular hypertrophy and hypertensive cardiomyopathy are substantially limiting the number of drugs that can be used for rhythm control. In most cases in the presence of hypertension initiation of anticoagulation therapy is necessary too.]