Clinical outcomes in patients with acute myocardial infarction treated with primary percutaneous coronary intervention stratified according to duration of pain-to-balloon time and type of myocardial infarction.

BACKGROUND: Based on the clinical outcomes of patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI), treated with primary percutaneous coronary intervention (pPCI), this study intended to assess mortality and major adverse cardiac and cerebrovascular event (MACCE) rates according to duration of pain-to-balloon (PTB) time and type of MI. METHODS: This is a retrospective cohort study based on the prospectively collected ORPKI registry which covers PCIs performed in Poland chosen between January 2014 and December 2017. Under assessment were 1,994 STEMI and 923 NSTEMI patients. Study endpoints included mortality and MACCE rates (in-hospital, 30-day, 12- and 36-month). Predictors of all-cause mortality in the overall group, STEMI and NSTEMI were assessed by multivariable analysis. RESULTS: Kaplan-Meier survival curve analysis did not reveal significant differences between the STEMI and NSTEMI group for all-cause mortality or MACCE at the 36-month follow-up. While in the long PTB time group, MACCE rate was significantly greater in STEMI patients when compared to NSTEMI (p = 0.004). Among STEMI patients, the short, medium and long PTB time groups differed significantly in the rate of all-cause mortality (p = 0.006) and MACCE (p = 0.04) at 1,095 days of follow-up, which were the greatest in the long PTB time group. CONCLUSIONS: Before considering the length of PTB time, there were no statistically significant differences in mortality or MACCE frequency between the STEMI and NSTEMI group at 36-month follow-up. Longer PTB times are related to significantly greater mortality at the 36-month follow-up in the STEMI, but not in the NSTEMI group.

Long-Term Prognostic Significance of High-Sensitive Troponin I Increase during Hospital Stay in Patients with Acute Myocardial Infarction and Non-Obstructive Coronary Arteries.

Background and Objectives: A topic already widely investigated is the negative prognostic value regarding the extent of high sensitive troponin I (hs-TnI) increases among patients with myocardial infarction (MI) and obstructive coronary atherosclerosis compared to a group of patients with MI and non-obstructive coronary atherosclerosis (MINOCA). Thus, the aim of this study was to evaluate the prognostic value concerning the extent of hs-TnI increase on clinical outcomes among patients with a MINOCA working diagnosis. Materials and Methods: We selected 337 consecutive patients admitted to hospital with a working diagnosis of MINOCA. The patients were divided in three groups according to the extent of hs-TnI increase during hospitalization (increase ≤5-times above the limit of the upper norm, >5 and ≤20-times, and >20-times). The study endpoints included all-cause mortality and major adverse cardiac and cerebrovascular events (MACCE; cerebral stroke and transient ischemic attacks, MI, coronary artery revascularization, either percutaneous coronary intervention or coronary artery bypass grafting and all-cause mortality). Results: During the mean follow-up period of 516.1 ± 239.8 days, using Kaplan-Meier survival curve analysis, significantly higher mortality rates were demonstrated among patients from the group with the greatest hs-TnI increase compared to the remaining groups (p = 0.01) and borderline values for MACCE (p = 0.053). Multivariable cox regression analysis did not confirm hs-TnI among factors related to increased MACCE or all-cause mortality rates. Conclusion: While a relationship between clinical outcomes and the extent of the hs-TnI increase among patients with a MINOCA working diagnosis remains, it does not seem to be not as strong as it is in patients with obstructive coronary atherosclerosis.

Effect of neutral endopeptidase inhibition on vascular response induced by exogenous angiotensin I in the isolated rat lung.

It is suggested that vasoconstriction mediated by angiotensin II cleaved from angiotensin I by angiotensin converting enzyme (ACE) is counterbalanced by concomitant formation of vasodilator angiotensin (1-7) by neutral endopeptidase (NEP). Here, we tested this hypothesis using as a bioassay the isolated rat lung perfused with Krebs-Henseleit (KH) solution and ventilated with negative pressures. Addition of angiotensin I (100 nM) into the isolated lung resulted in an immediate increase in pulmonary arterial pressure (Delta PAP) which was not accompanied by a significant change in respiratory lung function or weight of the lung. The Delta PAP response induced by angiotensin I was abolished by an inhibitor of ACE, perindoprilate (1 microM), or by angiotensin type 1 receptor antagonist (losartan, 1 microM) but not by angiotensin type 2 receptor antagonist (PD 123.319, 10 microM) suggesting the involvement of ACE and AT1 (but not AT2) receptors in this response. On the other hand, antagonist of bradykinin receptor B2 (icatibant, 100 nM) or an inhibitor of neutral endopeptidase, thiorphan (1 microM and 10 microM) did not modify DeltaPAP response induced by angiotensin I. In summary, in the isolated rat lung perfused with KH solution, ACE has a dominant role in the pulmonary conversion of angiotensin I to angiotensin II, while NEP-derived angiotensin 1-7 does not seem to constitute a major counterbalancing mechanism in the pulmonary vasoconstriction induced by endogenously formed angiotensin II.

Hypoxic pulmonary vasoconstriction in isolated blood-perfused rat lung; modulation by thromboxane A2, platelet-activating factor, cysteinyl leukotrienes and endothelin-1.

Recent evidence suggests that hypoxic pulmonary vasoconstriction (HPV) is mediated by hypoxia-induced closure of voltage-gated potassium channels in pulmonary vascular smooth muscle cells. It is also claimed that various vasoconstrictor mediators such as thromboxane A2 (TXA2), platelet activating factor (PAF), cysteinyl leukotrienes (cys-LTs) or endothelin-1 (ET-1) contribute to HPV. Their role, however, has not been unequivocally accepted. On the contrary, it is well known that endothelium-derived nitric oxide negatively modulates HPV. Since NO counteracts action of vasoconstrictor mediators, we tested the hypothesis that modulatory role of TXA2 PAF, cys-LTs and ET-1 in HPV would become apparent in absence of endogenous NO. For that purpose we assessed contribution of these mediators to HPV in the isolated blood-perfused rat lung pretreated with a non-selective NOS inhibitor, L-NAME. HPV, which was greatly augmented by L-NAME (300 microM) alone, was inhibited neither by a TXA2 synthase inhibitor (Camonagrel, 300 pM), nor by a PAF receptor antagonist (WEB 2170, 100 microM), nor by an inhibitor of five-lipooxygenase-activating protein (MK 886, 10 microM), nor by a non-selective ET-1 receptor antagonist (LU 302872, 30 pM). In summary, in isolated blood-perfused rat lung, TXA2, PAF, cys-LTs and ET-1 seem not to be involved in HPV, whereas we confirm the dominant role of endogenous NO in blunting HPV.