[Acute respiratory syndrome with various signs and outcomes caused by the SARS-CoV-2 virus is the biggest challenge facing health systems worldwide today. The renin-angiotensin-aldosterone and kinin-kallikrein systems and within these two endopeptidases (ACE and ACE2) play a crucial role in the developing clinical feature of COVID-19. Adverse effects of the ACE-stimulated Ang II/AT1R axis (oxidant, pro-inflammatory effect, vasoconstriction) are counterbalanced by the ACE2-induced AT2R and MasR activities (antioxidant, anti-inflammatory effect, vasodilation). The severity of SARS-CoV-2 pneumonia and systemic inflammation explains the impairment of ACE2 (as an important defence factor of the lungs) caused by the biding spike protein of the SARS-CoV-2, which decreases the ACE2 levels. In parallel, bradykinin production also increases and intensifies the SARS-CoV-2-induced cytokine storm through the BKB1 and BKB2 receptors. Since the RAAS inhibitors (ACEI, ARB) affect the two regulatory systems and enzymes at different sites and to different degrees, their role must urgently have been clarified in the COVID-19 since their use is essential and general of many population-wide diseases (hypertension, cardiovascular, renal and metabolic conditions). Based on pathophysiological and experimental data, it is reasonable to hypothesize that in COVID-19 with comorbidities, especially in the elderly, the decreased ACE2 expression may be restored by RAAS inhibitors and the missed or reduced protective effect may be revitalised. This protective effect applies to both RAAS inhibitors. Clinical trials clearly support the declared opinion of many international societies that the use of RAAS inhibitors does not increase the risk of the occurrence of SARS-CoV-2 in itself let alone the severe and critical cases. Accordingly, initiated RAAS inhibitor therapy not only may rather must be continued during the development of COVID-19.]

[The circadian (24-hour) variability of blood pressure (BP) is influenced by constant and variable (external and internal) factors. With this in mind and by determining the type of hypertension with a 24-hour blood pressure monitoring (ABPM), individual chronopharmacological (chronopharmacotherapy) treatment can be planned. There are significant differences in the chronokinetics of antihypertensive drugs administered at different times. Their therapeutic range and efficacy depend significantly on their circadian timing. Although the most modern antihypertensives have a 24-hour effect, they are not able to lower blood pressure at all times. Morning intake of ACE inhibitors, ARB-s, alpha-blockers mainly affect the afternoon and early evening rise, while evening intake reduces nocturnal and morning rise. Calcium channel blockers, beta-blockers (except carvedilol and labetolol), do not affect the circadian blood pressure profile. Therefore, in nondipper hypertension or in the case of morning rise, the twice daily morning and evening administration is more effective than the single morning administration. (Usually a lower dose is sufficient in the evening.) Adequate control of nocturnal or morning blood pressure elevations can be achieved with medication taken in the evening. According to the relevant studies the conclusion is that there is no convincing evidence that the administration of BP-lowering drugs in the evening provides any significant advantage in terms of quality of BP control, prevention of target organ damage or reduction of cardiovascular events, so evening intake only is not recommended. In particular the administration of antihypertensive drugs at bedtime, especially in the case of elderly patients may cause excessive BP fall at night with increased risk of silent cerebral infarct and the myocardial ischemia in patients with coronary heart disease.]

[The incidence and prevalence of heart failure (HF) is constantly increasing, its mor­bidity and mortality are still high, thus the disease burden is huge and its proper treatment is of paramount importance. Subs­tantial evidence on improving its prognosis remains available only by the treatment of chronic heart failure with reduced left ventricular function (HFrEF). There have been published a number of “milestone” studies in the last decades, the results of which fundamentally determined the HF therapy until recently. Baseline therapy for HFrEF has been placed on three pillars for a long time: angiotensin-converting-en­zyme inhibitors (ACEI), beta-blocker (BB), and mi­ne­ralocorticoid receptor antagonist (MRA) are included in different heart failure guide­lines with I/A level recommendation. The ground-breaking highly important PARADIGM-HF study was published in 2014, and examined an entirely new class of drugs, the sacubitril/valsartan, which belongs to the group of angiotensin receptor blocking/neprilysin inhibitors (ARNI) in HFrEF patients. Results of this study showed that sacubitril/valsartan significantly reduced the primary composite endpoint of CV mortality and HF hospitalization by 20% and reduced overall mortality by 16% compared to an active comparator enalapril, which has the broadest evidence in HFrEF therapy. The 2016 European Society of Cardiology (ESC) HF guidelines recommended the use of sacubitril/valsartan with an I/B evidence level as a replacement for an ACEI to further reducing the risk of HF hospitalization and death of out-patients with HFrEF who remained symptomatic despite optimal treatment with an ACEI, a BB and an MRA. Later, several smaller studies concerned sacubitril/valsartan with slightly different indications and in other patient groups. The PIONEER-HF study demonstrated that early initiation of sacubitril/valsartan therapy after the stabiliza­tion of acute HF is safe and effective in HFrEF patients, reduces more rapidly the NT-proBNP levels - which correlates with HF prognosis -, than the enalapril. The TRANSITION and TITRATION studies provided useful information on the initiation of sacubitril/valsartan therapy and the strategy of dose titration. The appearance of sacubitril/valsartan opened a new era in HFrEF therapy a few years ago, an era we are actually experiencing in Hungary. Thanks to SGLT-2 inhibitors, it is also possible that we are at the door of an even newer therapeutic era. This question is expected to be answered in the new ESC HF-guidelines to be published soon this year. ]

[Data of our 254 patients who were treated with rt-PA between 1st of Jan, 2011 and 31st of Dec, 2014 were processed. We focused on angioneurotic oedema as allergic complication of thrombolysis which caused life threatening respiratory obstruction in two cases. We describe these two patients’ history. Out of 254 patients six (2.3%) suffered angioneurotic edema caused respiratory obstruction in two (0.90%) cases. This occurrence is approximately 1.3-5.1% in literature. Five, out of six patients who suffered from angioneurotic oedema, had been treated with ACE inhibitors or ARB before. The role of ACE inhibitors is known in metabolism of bradykinin cascade. Plasmin which present during thrombolysis, precipitates biochemical mechanisms of this potential life threatening complication. Therefore rt-PA alone can be the cause of angioedema, but it can be more frequent together with ACE inhibitors therapy.]

[The rapporteur for the in-depth parliamentary debate was Gyula Fekete (MDF) from the Committee on Budget, Tax and Finance. He said that his committee had discussed the motions to amend the revenue and expenditure of the Budget and its balance with particular attention. ]