Authors
- Marijan Pašalić — University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-3197-2190
- Jure Samardžić — University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-9346-6402
- Boško Skorić — University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0001-5979-2346
- Maja Čikeš — University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-4772-5549
- Jana Ljubas Maček — University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0001-7171-2206
- Daniel Lovrić — University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-5052-6559
- Hrvoje Jurin — University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0002-2599-553X
- Davor Miličić — University Hospital Centre Zagreb, Zagreb, Croatia — ORCID: 0000-0001-9101-1570
Keywords
pulmonary hypertension, chronic systolic heart failure, left ventricular dysfunction, platelet function
DOI
https://doi.org/10.15836/ccar2018.366Full Text
Background: Role of platelets in the pathogenesis of primary pulmonary hypertension is well established. Platelets act as mediators of vasoconstriction, inflammation, coagulation and vascular remodeling, all of which result in changes to the pulmonary circulation. ( 1 - 3 ) Although being a more common entity, data on pathogenesis of pulmonary hypertension (PH) secondary to heart disease remain scarce. The aim of this study was to shed light on the importance platelets have in the pathogenesis of PH secondary to chronic systolic heart failure (CSHF). Patients and Methods: Measurement of platelet function was performed on 160 patients (57±10 years; 65% male) with CSHF admitted to University Hospital Centre Zagreb from October 2011 till October 2016. All patients were candidates for advanced treatment modalities and underwent right heart catheterization. Following the invasive measurement of hemodynamic parameters (including pulmonary artery pressure-PAP and vasoreactivity testing using alprostadil), blood samples were obtained from the pulmonary artery. Platelet aggregation induced by acetylsalicylic acid (ASPI), adenosine diphosphate (ADP), collagen (COL) or thrombin receptor activating peptide-6 (TRAP), was measured using Multiplate Analyzer. Results: Most common causes of CSHF were ischemic and dilated cardiomyopathy (ICMP 45% vs DCMP 43%). As expected, all patients presented with decreased cardiac index and PH due to elevated left ventricular filling pressure (PCWP) ( Table 1 ). Baseline aggregation tests showed reduced platelet activity, with ASPI being lower in patients with ICMP (p <0.001, due to acetylsalicylic acid therapy). COL test values were found to correlate significantly with PAP and PCWP ( Figure 1 ). Vasoreactivity testing was performed in 26% of patients, and positive in 53% of cases ( Table 2 ). Changes in PAP and PCWP correlated significantly with changes in ASPI and ADP tests ( Figure 2 ). Regression plots showing linear interrelation between collagen induced aggregation (COL) and mean pulmonary artery pressure (PAP), i.e. left ventricular filling pressure (PCWP). Regression plots showing linear interrelation between changes in acetylsalicylic acid induced aggregation (ASPI) and in mean pulmonary artery pressure (PAP), i.e. changes in ADP induced aggregation (ADP) and in left ventricular filling pressure (PCWP), following vasoreactivity testing with alprostadil. Conclusion: Platelets seems to play an important role in pathogenesis of PH secondary to CSHF. Further research on mechanisms and potential clinical significance of this interaction is warranted.