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Lege Artis Medicinae

JUNE 07, 2021

[Hypertension, COPD and COVID-19. Focus on antihypertensive therapy]


[Chronic obstructive pulmonary disease is a very common comorbidity of hypertension and it is often unrecognised by physicians. The factors involved in the pathomechanism of both diseases should be realised when choosing treatment. Among factors, hypoxia, increased tone of sympathetic nervous system and activation of renin-angiotensin-aldosterone system should primarily be considered. Vascular wall damage and endothelial dysfunction has an important role in both conditions. The goals of treatment are elimination of risk factors, optimizing the blood pressure, the consequential prevention of cardio-cerebrovascular, renal and pulmonary damage; finally prolonging the patients’ life and improving their quality of life as well. Both hypertension and COPD significantly worsen the condition of COVID-19 patients since they increase the severity of the disease and the rate of in-patients’ and their mortality. In the treatment of hypertension among COPD and COVID-19 patients there must be emphasized the medication inhibiting of renin-angiotensin-aldosterone system, such as angiotensin-converting en­zyme inhibitors or angiotensin-II AT1 re­cep­tor antagonists. Special attention concerned the beneficial effect of mineralocorticoid receptor antagonist spironolactone. Other antihypertensive drugs (calcium channel blockers, thiazide-like diu­retics, high selectivity β1 receptor antagonists) may supplement the treatment if necessary. Long-acting β2 receptor agonists, muscarinic receptor antagonists and inhalation corticosteroids may be administered in double or triple combination also in hypertension and COPD as well. It is important to note, that statin therapy and also vitamin D3 improve the condition of COVID-19 patients.]

Clinical Neuroscience

MARCH 30, 2016

[The importance of anticoagulant therapy in patients with artial fibrillation in stroke prevention – summary of international data and novel therapeutic modalities]


[The most common cardiogenic cause of ischaemic stroke is atrial fibrillation which increases the probability of stroke five-fold and doubles case fatality. Based on international data the incidence of atrial fibrillation is approx. 2% however this rapidly increases with age. The necessity of using oral anticoagulants in the prevention of non-valvular atrial fibrillation related stroke is decided based on estimated stroke risk. The CHADS2 and the more predictive CHA2DS2-VASc scales are used for this purpose while the bleeding risk of patients treated with anticoagulant may be estimated by the HAS-BLED scoring scale. For decades oral anticoagulation meant using vitamin-K antagonists. Based on international data we can see that rate of anticoagulation is unacceptably low, furthermore most of the anticoagulated patients aren’t within the therapeutic range of INR (INR: 2-3). A lot of disadvantages of vitamin-K antagonists are known (e.g. food-drug interaction, need for regular coagulation monitoring, increased risk of bleeding), therefore compounds with new therapeutic target have been developed. The novel oral anticoagulants (NOAC) can be divided in two major subgroups: direct thrombin inhibitors (dabigatran etexilate) and Xa-factor inhibitors (rivaroxaban, apixaban, edoxaban). These products are administered in fix doses, they less frequently interact with other medications or food, and regular coagulation monitoring is not needed when using these drugs. Moreover several studies have shown that they are at least as effective in the prevention of ischaemic stroke than the vitamin-K antagonists, with no more haemorrhagic complications.]

Lege Artis Medicinae

OCTOBER 01, 2000

[Molecular mechanisms of cardiac hypertrophy and heart failure]

MIKALA Gábor, PETŐ Mónika, VÁLYI Nagy István, CSÁSZÁR Albert

[In this review, the most important molecular mechanisms leading to cardiac muscle hypertrophy and consequentially to heart failure are detailed. In numerous instances, understanding molecular mechanisms offers the possibility for pharmacotherapeutic intervention. First, trimeric G-proteins and their attached intracellular signaling pathways are introduced, with special emphasis on the pathways elucidated by transgenic animal models. In this area, there are several clinically effective drugs to influence cardiac hypertrophy, including ACE inhibitors, angiotensin receptor antagonists, as well as a- and B-adrenergic receptor blockers. Mitogen activated protein kinases participate later in the hypertrophic cascade. There are ongoing investigations on the potential therapeutic use of lipid-soluble statins these are indirect inhibitors of Ras-farnesylation. Altered cellular Ca2+-homeostasis is fundamental with respect to cardiac muscle hypertrophy and heart failure. The third part of this article investigates the role of the calcium/calmodulin dependent protein phosphatase called calcineurin in these processes. Administration of cyclosporin A or tacrolimus (both are inhibitors of calcineurin) may not be recommended in most forms of cardiac hypertrophy, however, in certain settings they may prove to be valuable therapeutic agents. One of the most serious, not yet properly addressed problem of late stage heart failure is the development of ventricular arrhythmias caused by repolarization abnormalities. Certain mechanisms of this phenomenon are highlighted with a special note on Nat-Cat exchange inhibitors as one of future therapeutic agents of much promise. ]

Thrombosis management

APRIL 27, 2020

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.]