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Background Concomitant vasoactive drugs are often required to maintain adequate perfusion pressure in patients with acute myocardial infarction (AMI) and cardiogenic shock (CS) receiving hemodynamic support with an axial flow pump (Impella CP). Objective To compare the effect of equipotent dosages of epinephrine, dopamine, norepinephrine, and phenylephrine on cardiac work and end-organ perfusion in a porcine model of profound ischemic CS supported with an Impella CP. Methods CS was induced in 10 pigs by stepwise intracoronary injection of polyvinyl microspheres. Hemodynamic support with Impella CP was initiated followed by blinded crossover to vasoactive treatment with norepinephrine (0.10 μg/kg/min), epinephrine (0.10 μg/kg/min), or dopamine (10 μg/kg/min) for 30 min each. At the end of the study, phenylephrine (10 μg/kg/min) was administered for 20 min. The primary outcome was cardiac workload, a product of pressure-volume area (PVA) and heart rate (HR), measured using the conductance catheter technique. End-organ perfusion was assessed by measuring venous oxygen saturation from the pulmonary artery (SvO 2 ), jugular bulb, and renal vein. Treatment effects were evaluated using multilevel mixed-effects linear regression. Results All catecholamines significantly increased LV stroke work and cardiac work, dopamine to the greatest extend by 341.8 × 10 3 (mmHg × mL)/min [95% CI (174.1, 509.5), p  < 0.0001], and SvO 2 significantly improved during all catecholamines. Phenylephrine, a vasoconstrictor, caused a significant increase in cardiac work by 437.8 × 10 3 (mmHg × mL)/min [95% CI (297.9, 577.6), p  < 0.0001] due to increase in potential energy ( p  = 0.001), but no significant change in LV stroke work. Also, phenylephrine tended to decrease SvO 2 ( p  = 0.063) and increased arterial lactate levels ( p  = 0.002). Conclusion Catecholamines increased end-organ perfusion at the expense of increased cardiac work, most by dopamine. However, phenylephrine increased cardiac work with no increase in end-organ perfusion.

Aims Veno‐arterial extracorporeal membrane oxygenation (VA‐ECMO) with profound left ventricular (LV) failure is associated with inadequate LV emptying. To unload the LV, VA‐ECMO can be combined with Impella CP (ECMELLA). We hypothesized that ECMELLA improves cardiac energetics compared with VA‐ECMO in a porcine model of cardiogenic shock (CS). Methods and results Land‐race pigs (weight 70 kg) were instrumented, including a LV conductance catheter and a carotid artery Doppler flow probe. CS was induced with embolization in the left main coronary artery. CS was defined as reduction of ≥50% in cardiac output or mixed oxygen saturation (SvO2) or a SvO2 < 30%. At CS VA‐ECMO was initiated and embolization was continued until arterial pulse pressure was <10 mmHg. At this point, Impella CP was placed in the ECMELLA arm. Support was maintained for 4 h. CS was induced in 15 pigs (VA‐ECMO n = 7, ECMELLA n = 8). At time of CS MAP was <45 mmHg in both groups, with no difference at 4 h (VA‐ECMO 64 mmHg ± 11 vs. ECMELLA 55 mmHg ± 21, P = 0.08). Carotid blood flow and arterial lactate increased from CS and was similar in VA‐ECMO and ECMELLA [239 mL/min ± 97 vs. 213 mL/min ± 133 (P = 0.6) and 5.2 ± 3.3 vs. 4.2 ± 2.9 mmol/ (P = 0.5)]. Pressure‐volume area (PVA) was significantly higher with VA‐ECMO compared with ECMELLA (9567 ± 1733 vs. 6921 ± 5036 mmHg × mL/min × 10−3, P = 0.014). Total diureses was found to be lower in VA‐ECMO compared with ECMELLA [248 mL (179–930) vs. 506 mL (418–2190); P = 0.005]. Conclusions In a porcine model of CS, we found lower PVA, with the ECMELLA configuration compared with VA‐ECMO, indicating better cardiac energetics without compromising systemic perfusion.

Background Low systolic blood pressure (SBP) is a key criterion for diagnosing cardiogenic shock (CS) caused by a reduction in stroke volume and cardiac output (CO). The temporal interaction between changes in pressure and flow has not been well described in the development of CS. In a large animal model, we assessed the temporal relationships of SBP, CO, and blood flow in the carotid artery during induction of CS. Methods Fifteen adult Danish landrace pigs (median weight 71 kg) underwent CS induction by stepwise injection of polyvinyl alcohol microspheres into the left main coronary artery every 3 min to induce microvascular obstruction. After each injection, CO, SBP, and mixed venous saturation (SvO 2 ) were recorded simultaneously from a ventricle sheath in the carotid artery and a pulmonary artery catheter in the right internal jugular vein. A Doppler flow probe measured blood flow in the left carotid artery. CS was defined as a ≥ 50% reduction in CO or SvO 2 from baseline, or absolute SvO 2  < 30%. Results CS occurred after a mean of 8 (range 5 to 19) boluses of microspheres. SBP declined from 99 (± 15) mmHg to 74 (± 6) mmHg, equal to 74 (± 13)% of the baseline value. CO was reduced to 5.8 (± 0.7) L/min to 2.2 (± 1.3) L/min, equal to 38 (± 23)% and SvO 2 from 63 (± 7)% to 37 (± 7)%, equal to 60 (± 13)% of baseline values. The decrease in CO was due to a reduction to 43 (± 26)% in stroke volume, as heart rate remained unchanged. The carotid artery blood flow was reduced from 285 (± 50) mL/min to 155 (± 56) mL/min, equal to 54% of baseline values. The decline in SvO 2 and CO preceded a reduction in SBP, and after 25% of emboli were given, CO decreased by 24% while SBP was unchanged. Conclusion In a porcine model of ischemic myocardial injury, the decrease in blood flow and stroke volume preceded a decline in SBP, suggesting pressure preservation occurs in the presence of hypoperfusion.

We sought to examine the relation between sodium bicarbonate prophylaxis for contrast-associated nephropathy (CAN) and mortality. We conducted an individual patient data meta-analysis from multiple randomized controlled trials. We obtained individual patient data sets for 7 of 10 eligible trials (2,292 of 2,764 participants). For the remaining 3 trials, time-to-event data were imputed based on follow-up periods described in their original reports. We included all trials that compared periprocedural intravenous sodium bicarbonate to periprocedural intravenous sodium chloride in patients undergoing coronary angiography or other intra-arterial interventions. Included trials were determined by consensus according to predefined eligibility criteria. The primary outcome was all-cause mortality hazard, defined as time from randomization to death. In 10 trials with a total of 2,764 participants, sodium bicarbonate was associated with lower mortality hazard than sodium chloride at 1 year (hazard ratio 0.61, 95% confidence interval [CI] 0.41 to 0.89, p = 0.011). Although periprocedural sodium bicarbonate was associated with a reduction in the incidence of CAN (relative risk 0.75, 95% CI 0.62 to 0.91, p = 0.003), there exists a statistically significant interaction between the effect on mortality and the occurrence of CAN (hazard ratio 5.65, 95% CI 3.58 to 8.92, p <0.001) for up to 1-year mortality. Periprocedural intravenous sodium bicarbonate seems to be associated with a reduction in long-term mortality in patients undergoing coronary angiography or other intra-arterial interventions.

BackgroundIn selected cases of cardiogenic shock, veno-arterial extracorporeal membrane oxygenation (V-A ECMO) is combined with trans valvular micro axial flow pumps (ECMELLA). Observational studies indicate that ECMELLA may reduce mortality but exposing the patient to two advanced mechanical support devices may affect the early inflammatory response. We aimed to explore inflammatory biomarkers in a porcine cardiogenic shock model managed with V-A ECMO or ECMELLA.MethodsFourteen landrace pigs had acute myocardial infarction-induced cardiogenic shock with minimal arterial pulsatility by microsphere embolization and were afterwards managed 1:1 with either V-A ECMO or ECMELLA for 4 h. Serial blood samples were drawn hourly and analyzed for serum concentrations of interleukin 6 (IL-6), IL-8, tumor necrosis factor alpha, and serum amyloid A (SAA).ResultsAn increase in IL-6, IL-8, and SAA levels was observed during the experiment for both groups. At 2–4 h of support, IL-6 levels were higher in ECMELLA compared to V-A ECMO animals (difference: 1416 pg/ml, 1278 pg/ml, and 1030 pg/ml). SAA levels were higher in ECMELLA animals after 3 and 4 h of support (difference: 401 ng/ml and 524 ng/ml) and a significant treatment-by-time effect of ECMELLA on SAA was identified (p = 0.04). No statistical significant between-group differences were observed in carotid artery blood flow, urine output, and lactate levels.ConclusionsLeft ventricular unloading with Impella during V-A ECMO resulted in a more extensive inflammatory reaction despite similar end-organ perfusion.

We compared 5-year clinical outcomes in diabetic and nondiabetic patients treated with Endeavor zotarolimus-eluting stents (ZESs; Endeavor Sprint, Medtronic, Santa Rosa, California) or Cypher sirolimus-eluting stents (SESs; Cordis, Johnson & Johnson, Warren, New Jersey) coronary implantation. We randomized 2,332 patients to either ZESs (n = 1,162, n = 169 diabetic patients) or SESs (n = 1,170, n = 168 diabetic patients) stratified according to presence or absence of diabetes mellitus. End points included major adverse cardiac event (MACE), a composite of cardiac death, myocardial infarction, target vessel revascularization (TVR), and definite stent thrombosis. Among diabetic patients, MACE occurred more frequently in patients treated with ZESs than SESs (48 [28.4%] vs 31 [18.5%]; odds ratio [OR] 1.75, 95% confidence interval [CI] 1.05 to 2.93, p = 0.032) because of a higher rate of TVR (32 [18.9%] vs 14 [8.3%]; OR 2.57, 95% CI 1.32 to 5.02, p = 0.006). Among nondiabetic patients, ZES and SES had similar MACE rates at 5-year follow-up but SES was associated with a significantly higher risk of definite stent thrombosis (10 [1.0%] vs 23 [2.3%]; OR 0.43, 95% CI 0.20 to 0.91, p = 0.028). Moreover, during the last 4 years, ZES had fewer MACE, TVR, and stent thrombosis events among nondiabetic patients. In conclusion, SES remains superior to ZES in patients with diabetes throughout the 5-year follow-up, however, among nondiabetic patients, SES demonstrated a highly dynamic performance with favorable initial results followed by a late catch-up that included an overall higher risk of stent thrombosis.

Registry studies and case-control studies have demonstrated that the risk of acute myocardial infarction (AMI) is increased following influenza infection. Small randomized trials, underpowered for clinical end points, indicate that future cardiovascular events can be reduced following influenza vaccination in patients with established cardiovascular disease. Influenza vaccination is recommended by international guidelines for patients with cardiovascular disease, but uptake is varying and vaccination is rarely prioritized during hospitalization for AMI. The Influenza vaccination After Myocardial Infarction (IAMI) trial is a double-blind, multicenter, prospective, registry-based, randomized, placebo-controlled, clinical trial. A total of 4,400 patients with ST-segment elevation myocardial infarction (STEMI) or non-STEMI undergoing coronary angiography will randomly be assigned either to in-hospital influenza vaccination or to placebo. Baseline information is collected from national heart disease registries, and follow-up will be performed using both registries and a structured telephone interview. The primary end point is a composite of time to all-cause death, a new AMI, or stent thrombosis at 1 year. The IAMI trial is the largest randomized trial to date to evaluate the effect of in-hospital influenza vaccination on death and cardiovascular outcomes in patients with STEMI or non-STEMI. The trial is expected to provide highly relevant clinical data on the efficacy of influenza vaccine as secondary prevention after AMI.

In-stent restenosis (ISR) still occurs after percutaneous coronary intervention (PCI). Few studies have compared the outcomes of PCI for de novo stenosis with those of PCI for ISR, and the results are conflicting. The present study aimed to conduct this comparison. Using patient-level data from the randomized all-comer SORT OUT studies III to X, we included all patients with previous PCI and either an ISR or a de novo lesion as the study target lesion. Outcomes of interest were major adverse cardiac events (MACE) and target lesion revascularization (TLR) after 5 years. Of the 2,928 patients with a previous PCI included in the SORT OUT studies, 491 (17%) were treated for ISR and 2,437 (83%) for a de novo stenosis. Baseline characteristics did not differ significantly. At 5 years, MACE occurred in 148 patients (32%) in the ISR group and 654 patients (28%) in the de novo stenosis group (crude and adjusted hazard ratio 1.16 [95% confidence interval (CI) 0.97 to 1.38] and 1.16 [95% CI 0.97 to 1.38]). The risk of TLR was higher in the ISR group compared with the de novo stenosis group (crude and adjusted hazard ratio 1.64 [95% CI 1.24 to 2.17] and 1.71 [95% CI 1.27 to 2.30]). In conclusion, the risk of MACE was similar between PCI for ISR and PCI for de novo lesions after 5 years. However, the risk of TLR was higher in the ISR group compared with the de novo stenosis group.

In patients with STEMI with cardiogenic shock, early mechanical support with a microaxial pump reduced the risk of death at 180 days, with the survival benefit persisting up to 10 years despite device-related complications.

Influenza vaccination early after myocardial infarction (MI) improves prognosis but vaccine effectiveness may differ dependent on type of MI. A total of 2,571 participants were prospectively enrolled in the Influenza vaccination after myocardial infarction (IAMI) trial and randomly assigned to receive in-hospital inactivated influenza vaccine or saline placebo. The trial was conducted at 30 centers in eight countries from October 1, 2016 to March 1, 2020. Here we report vaccine effectiveness in the 2,467 participants with ST-segment elevation MI (STEMI, n = 1,348) or non-ST-segment elevation MI (NSTEMI, n = 1,119). The primary endpoint was the composite of all-cause death, MI, or stent thrombosis at 12 months. Cumulative incidence of the primary and key secondary endpoints by randomized treatment and NSTEMI/STEMI was estimated using the Kaplan-Meier method. Treatment effects were evaluated with formal interaction testing to assess for effect modification. Baseline risk was higher in participants with NSTEMI. In the NSTEMI group the primary endpoint occurred in 6.5% of participants assigned to influenza vaccine and 10.5% assigned to placebo (hazard ratio [HR], 0.60; 95% CI, 0.39-0.91), compared to 4.1% assigned to influenza vaccine and 4.5% assigned to placebo in the STEMI group (HR, 0.90; 95% CI, 0.54-1.50, P = .237 for interaction). Similar findings were seen for the key secondary endpoints of all-cause death and cardiovascular death. The Kaplan-Meier risk difference in all-cause death at one year was more pronounced in participants with NSTEMI (NSTEMI: HR, 0.47; 95% CI 0.28-0.80, STEMI: HR, 0.86; 95% CI, 0.43-1.70, interaction P = .028). The beneficial effect of influenza vaccination on adverse cardiovascular events may be enhanced in patients with NSTEMI compared to those with STEMI.