ObjectivesTo determine whether the extent of myocardial fibrosis by late-gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR), and echocardiographic ventricular dyssynchrony can independently predict response to medical therapy in patients with newly-diagnosed idiopathic dilated cardiomyopathy (DCM).
Pulmonary hypertension associated with left-sided heart disease (PH-LHD) is the most common type of pulmonary hypertension. In patients with left-sided heart disease, the presence of pulmonary hypertension is typically a marker of more advanced disease, more severe symptoms, and worse prognosis. In contrast to pulmonary arterial hypertension, PH-LHD is characterised by an elevated pulmonary artery wedge pressure (postcapillary pulmonary hypertension) without or with an additional precapillary component (isolated postcapillary vs combined postcapillary and precapillary pulmonary hypertension). Transthoracic echocardiography is the primary noninvasive imaging tool to estimate the probability of pulmonary hypertension and to establish a working diagnosis on the mechanism of pulmonary hypertension. However, right heart catheterisation is always required if significant pulmonary hypertension is suspected and exact knowledge of the haemodynamic constellation is necessary. The haemodynamic constellation (mean pulmonary artery pressure, mean pulmonary artery wedge pressure, left ventricular end-diastolic pressure) in combination with clinical information and imaging findings (mainly echocardiography, coronary angiography and cardiac magnetic resonance imaging) will usually allow the exact mechanism underlying PH-LHD to be defined, which is a prerequisite for appropriate treatment. The general principle for the management of PH-LHD is to treat the underlying left-sided heart disease in an optimal manner using drugs and/or interventional or surgical therapy. There is currently no established indication for pulmonary arterial hypertension-specific therapies in PH-LHD, and specific therapies may even cause harm in patients with PH-LHD.
Spontaneous coronary artery dissection (SCAD) is an increasingly diagnosed cause of acute myocardial infarction. However, there is still a limited number of larger cohorts with long-term follow-up. We report on the largest Swiss single-centre cohort to date, with follow-up of up to 22 years.We prospectively collected SCAD cases from June 1998 until December 2020. A strategy of systematic follow-up angiography was applied. Information on long-term follow-up was collected up to the end of 2020. Major cardiovascular events (MACE) were defined as all-cause death, non-fatal MI, and non-fatal cardiac arrest.We identified 105 SCAD patients (mean age 53 ± 11 years, 98 female, 5 peripartum). Presentation was myocardial infarction in all patients. In 102 patients, there was one contiguous dissection. Three patients had two (n = 2) or three (n = 1) non-contiguous dissections. In the majority of patients (n = 97), the primary treatment approach was conservative (dual antiplatelet therapy for 12 months in 90% of patients, statins in 91%). Seven patients were treated with percutaneous coronary intervention (PCI) and one patient underwent bypass surgery. Elective follow-up angiograms were performed in 73 asymptomatic patients after a median follow-up of 6.0 months (interquartile range [IQR] 5.5-6.5). These showed healing of the dissection (n = 65) or a good result after PCI (n = 5) in 70 patients. Three patients had a persistent dissection but conservative treatment was continued. After a median follow-up of 7.5 years (IQR 3.6-12.5) (longest follow-up: 22.5 years) there were 15 MACE. Five MACE occurred within 30 days of the index event: death following catastrophic peripartum left main SCAD (n = 1), out-of-hospital cardiac arrest with successful resuscitation 16 days after SCAD (n = 1), ST-segment elevation myocardial infarction due to occlusion of the dissected artery 10 hours after the index angiogram with subsequent PCI (n = 1), SCAD of a second vessel 8 days after the index SCAD (n = 1), and non-ST-segment elevation myocardial infarction with persistent, multisite SCAD 10 days after the index event (n = 1). There were 10 late MACE, including myocardial infarction and recurrent SCAD (different vessel/lesion) a median of 7.6 years (IQR 3.9-9.6) after the index event in eight patients and death with unclear cause in two patients.This SCAD series highlights its highly variable clinical course during the acute phase and in the long term. Although most SCAD patients can be treated conservatively with subsequent healing of the dissection and good clinical outcome, there are also patients with dramatic acute presentation or MACE several years after the initial presentation.
Abstract Background The new 2018 pulmonary hypertension (PH) definition includes a lower mean pulmonary artery pressure (mPAP) cut‐off (>20 mmHg rather than ≥25 mmHg) and the compulsory requirement of a pulmonary vascular resistance (PVR) ≥3 Wood units (WU) to define precapillary PH. We assessed the clinical impact of the 2018 compared to the 2015 PH definition in aortic stenosis (AS) patients undergoing aortic valve replacement (AVR). Methods Severe AS patients (n = 487) undergoing pre‐AVR right heart catheterization were classified according to the 2015 and 2018 definitions. Post‐AVR mortality (median follow‐up 44 months) was assessed. Results Based on the 2015 definition, 66 (13%) patients exhibited combined pre and postcapillary PH (CpcPH), 116 (24%) isolated post‐capillary PH (IpcPH), 28 (6%) precapillary PH, and 277 (57%) no PH at all. Overall, 52 (11%) patients were reclassified: 23 no PH into IpcPH; 8 no PH into precapillary PH; 20 precapillary PH into no PH; 1 CpcPH into IpcPH. By the 2015 definition, only CpcPH patients displayed increased mortality, whereas by the 2018 definition, precapillary PH patients also experienced higher mortality than those without PH. Among the PH definition components, PVR ≥3 WU was the strongest predictor of death (hazard ratio > 4). Conclusions In severe AS, a higher number of IpcPH patients are diagnosed by the 2018 definition, even though they have the same prognosis as those without PH. Patients with true precapillary PH are more accurately identified by the 2018 definition that includes a pulmonary vascular disease criterion, that is, PVR ≥3 WU, a strong mortality predictor.
Differentiation between precapillary and postcapillary pulmonary hypertension (PH) classically relies on mean pulmonary artery wedge pressure (mPAWP). The left ventricular end-diastolic pressure (LVEDP) is proposed as an equivalent alternative. However, mPAWP and LVEDP may differ substantially. We compared the impact of the choice of using the mPAWP vs the LVEDP on PH classification and mortality prediction in patients with severe aortic stenosis (AS) undergoing valve replacement.In 335 patients with severe AS , both mPAWP and LVEDP were measured. A mean pulmonary artery pressure ≥ 25 mm Hg was used to define PH, and either mPAWP or LVEDP was used to differentiate between precapillary and postcapillary PH (≤ 15 vs > 15 mm Hg). Mortality after a median follow-up of 1484 days after aortic valve replacement was assessed.Overall, mPAWP was lower than LVEDP (16 ± 8 mm Hg vs 21 ± 8 mm Hg; P < 0.001). Among 140 patients (42%) with PH, the PAWP-based classification revealed 76 (54% of those with PH) with isolated postcapillary PH, 48 (34%) with combined pre- and postcapillary PH, and 16 (12%) with precapillary PH. When the LVEDP was used, 59 patients (42%) were differently classified. These patients had higher mortality than those who were not differently classified [hazard ratio 2.79 (95% confidence interval, 1.17-6.65); P = 0.02]. Higher mPAWP was associated with increased mortality [hazard ratio 1.07 (95% confidence interval, 1.03-1.11) per 1 mm Hg; P = 0.001], whereas higher LVEDP was not.Use of LVEDP rather than mPAWP results in a divergent PH classification in nearly every second patient with severe AS. These patients have higher mortality after aortic valve replacement. The mPAWP, but not the LVEDP, predicts mortality.La différentiation entre l’hypertension pulmonaire (HP) précapillaire et postcapillaire repose traditionnellement sur la pression artérielle pulmonaire d’occlusion moyenne (PAPOm). La pression télédiastolique du ventricule gauche (PTDVG) est proposée comme alternative équivalente. Toutefois, la PAPOm et la PTDVG peuvent largement différer. Nous avons comparé les répercussions du choix entre l’utilisation de la PAPOm vs l’utilisation de la PTDVG sur la classification de l’HP et la prédiction de la mortalité des patients atteints d’une sténose aortique (SA) grave qui subissaient un remplacement valvulaire.Nous avons mesuré la PAPOm et la PTDVG de 335 patients atteints de SA grave. Nous avons utilisé une pression artérielle pulmonaire moyenne ≥ 25 mmHg pour définir l’HP, et utilisé la PAPOm ou la PTVDG pour différencier entre l’HP précapillaire et postcapillaire (≤ 15 mmHg vs > 15 mmHg). Nous avons évalué la mortalité après un suivi médian de 1 484 jours après le remplacement valvulaire aortique.Dans l’ensemble, la PAPOm était plus faible que la PTVDG (16 ± 8 mmHg vs 21 ±8 mmHg; P < 0,001). Parmi les 140 patients (42 %) atteints d’HP, la classification en fonction de la PAPO a révélé 76 (54 % des patients atteints d’HP) patients atteints d’HP postcapillaire isolée, 48 (34 %) patients atteints d’HP précapillaire et postcapillaire combinée et 16 (12 %) patients atteints d’HP précapillaire. Lorsque nous avons utilisé la PTVDG, 59 patients (42 %) étaient classifiés différemment. La mortalité chez ces patients était plus élevée que chez les patients qui n’étaient pas classifiés différemment (rapport de risque 2,79 [intervalle de confiance à 95 %, 1,17-6,65]; P = 0,02). La PAPOm plus élevée était associée à une mortalité accrue (rapport de risque 1,07 [intervalle de confiance à 95 %, 1,03-1,11] par 1 mmHg; P = 0,001), tandis que la PTVDG plus élevée ne l’était pas.Le fait d’utiliser la PTVDG plutôt que la PAPOm entraîne une classification divergente de l’HP chez presque tous les deux patients atteints de SA grave. La mortalité après le remplacement valvulaire aortique de ces patients est plus élevée. La PAPOm, mais non la PTVDG, prédit la mortalité.
