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. 2022 Mar 11;11(6):1549. doi: 10.3390/jcm11061549

Table 1.

Patients’ characteristics and management.

Baseline Characteristics N = 392
Age (years) 73 ± 10.2
Age > 75 (years) 191 (48.7)
Female sex (%) 121 (30.9)
Prior HF hospitalisation 125 (31.9)
History of chronic heart failure 214 (54.6)
Systolic blood pressure at admission (mmHg) 131 ± 41.2
Heart rate at admission (beats/min) 87 ± 25.9
Smoking status (%)
   Non-smoker 224 (57.1)
   Former smoker 126 (32.2)
   Current smoker 42 (10.7)
Hypertension * 329 (83.9)
Type of diabetes
   Type 1 12 (3.1)
   Type 2 378 (96.4)
   Secondary (chronic pancreatitis) 2 (0.5)
HbA1c (%) 7.38 ± 1.48
Total cholesterol (mg/dL) 159 ± 57
LDL cholesterol (mg/dL) 96 ± 48
HDL cholesterol (mg/dL) 42 ± 16
TG (mg/dL) 262 ± 209
BMI (kg/m2) 29.1 ± 6.5
Family history of CAD (%) 33 (8.4)
Personal history of CAD (%) 163 (41.6)
Atrial fibrillation 76 (19.4)
Chronic respiratory failure (%) 96 (24.5)
eGFR (mL/min/1.73 m2) † 55.1 ± 29.2
CKD with RRT (%) 8 (2.0)
Left ventricular ejection fraction (LVEF) (%) 43.3 ± 13.0
   LVEF < 30% 81 (20.7)
   LVEF 30–40% 72 (18.4)
   LVEF 40–49% 95 (24.2)
   LVEF ≥ 50% 144 (36.7)
Pre-existent aetiologies of cardiopathies predisposing to AHF
   Ischaemic heart disease 142 (36.2)
   Toxic damage 19 (4.8)
   Immune-mediated and inflammatory damage 2 (0.5)
   Infiltration 2 (0.5)
   Metabolic derangements 5 (1.3)
   Genetic abnormalities 20 (5.1)
   Valve and myocardium structural defects 102 (26.0)
   Pericardial and endomyocardial pathologies 5 (1.3)
   Tachycardia-induced cardiomyopathy 7 (1.8)
   Prior HF hospitalisation in patient with preserved LVEF 36 (9.2)
   No pre-existent cardiopathy 52 (13.3)
Factors triggering AHF
   Acute coronary syndrome (ACS) 159 (40.6)
   Myocardial rupture complicating ACS ‡ 3 (0.7)
   Hypertensive emergency 40 (10.2)
   Tachyarrhythmia 50 (12.8)
   Bradyarrhythmia 12 (3.1)
   Acute native or prosthetic valve incompetence § 27 (6.9)
   Vigorous fluid administration 10 (7.7)
   Non-adherence with salt/fluid intake or medications 32 (8.2)
   Worsening renal failure 20 (5.1)
   Severe anaemia ¶ 20 (5.1)
   Infection (e.g., pneumonia, sepsis) 76 (19.4)
   Stress-related cardiomyopathy 3 (0.7)
   Metabolic/hormonal derangements # 7 (1.8)
   Toxic substances, cardiodepressant and other drugs ** 5 (1.3)
BNP value at admission (pg/mL) 597 (348–1300)
Arterial pH at admission (n = 200) 7.35 ± 0.11
Arterial blood lactate at admission (mmol/L) (n = 200) 2.35 ± 2.57
Acute kidney failure †† (%) 145 (37.0)
Cardiogenic shock ‡‡ 52 (13.3)
Peak troponin I (ng/mL) (normal < 0.04) §§ 0.34 (0.09–6)
Presence and extent of CAD (%)
   No invasive angiography 174 (44.4)
   No CAD 22 (5.6)
   No significant stenosis 44 (11.2)
   One-vessel disease 40 (10.2)
   Two-vessel disease 44 (11.2)
   Left main and/or three-vessel disease 68 (17.4)
   SYNTAX score 20.0 ± 13.2
GRACE Score (n = 159) 168 ± 37
GRACE Score > 140 118 (74.2)
Management
   Oxygen therapy 385 (98.2)
   Diuretics 375 (95.7)
   Intravenous vasodilators 104 (26.5)
   Inotropic agents ¶¶ 65 (16.6)
   Vasopressors ## 43 (11.0)
   Non-invasive positive pressure ventilation 114 (29.1)
   Mechanical ventilation 47 (12.0)
   Duration of mechanical ventilation (days) 3.3 ± 5.6
   Renal replacement therapy 34 (8.7)
   Intra-aortic balloon pump 8 (2.0)
   Mechanical circulatory support *** 10 (2.6)
   Heart transplantation 2 (0.5)
Myocardial revascularisation
   PCI 126 (32.1)
   CABG 23 (5.9)
   Hybrid strategy 2 (0.5)
   Medical treatment only ††† 8 (2.0)
Electrical cardioversion 20 (5.1)
Ablation for arrhythmias 5 (1.2)
Pacemaker 14 (3.6)
Non-surgical device treatment of heart failure
   Cardiac resynchronisation therapy 9 (2.3)
   Implantable cardioverter-defibrillator 5 (1.2)
Valvular heart disease treatment
   Trans-aortic valve replacement 14 (3.6)
   Valve surgery 22 (5.6)
Treatment at hospital discharge
   Diuretics 301 (76.8)
   RAASI 241 (61.5)
   ARNi 5 (1.2)
   ß-Blocker 260 (66.3)
   Mineralocorticoid antagonists 124 (31.6)
   Antithrombotic treatment (%)
    Single APT (SAPT) 77 (19.6)
    DAPT 96 (24.5)
    OAC monotherapy 75 (19.1)
    Dual therapy (OAC + SAPT) 62 (15.8)
    Triple therapy (OAC + DAPT) 27 (6.9)
   Statin 269 (68.6)
   Oral glucose-lowering therapies 197 (50.3)
    Biguanides 116 (29.6)
    Sulfonylureas and meglitinides 123 (31.4)
    α-glucosidase inhibitors 5 (1.2)
    DDP-4 inhibitors 49 (12.5)
    GLP-1 receptor agonists 5 (1.2)
   Insulin therapy 193 (49.2)
Glycaemic status
   Glycaemia assays per patient 45 (23–78)
   Glycaemia assays per patient per day 5 (3–8)
   Admission glycaemia (mg/dL) 193 (87)
   Mean glycaemia (mg/dL) 164 (32)
   Percentage of hypoglycaemia ‡‡‡ (%) 0.9
   Number of patients with hypoglycaemia (%) 84 (21.4)
   Hypoglycaemia events per patient, n 2 (1–2)
   Percentage of hyperglycaemia §§§ (%) 32.6
   Number of patients with hyperglycaemia (%) 357 (91.1)
   Glycaemic variability (SD, mg/dL) 53 (22)

Data shown are number (%), median (25th–75th percentiles) or mean ± SD. ACS: acute coronary syndrome; AHF: acute heart failure; APT: antiplatelet therapy; ARNi: angiotensin receptor-neprilysin inhibitor; BNP: B-type natriuretic peptide; BMI: body mass index; CABG: coronary artery bypass graft surgery; CAD: coronary artery disease; CKD with RRT: chronic kidney disease to renal replacement therapy; DAPT: dual antiplatelet therapy; eGFR: estimated glomerular filtration rate; GRACE: Global Registry of Acute Coronary Events; HDL: high-density lipoprotein; HF: heart failure; LDL: low-density lipoprotein; LVEF: left ventricular ejection fraction; OAC: oral anticoagulation therapy; PCI: percutaneous coronary intervention; RAASI: renin-angiotensin-aldosterone system inhibitors; SAPT: single antiplatelet therapy; SYNTAX: Synergy between PCI with Taxus and Cardiac Surgery. TG: triglyceride. * Hypertension was defined as systolic blood pressure ≥ 140 mmHg and/or diastolic blood pressure ≥ 90 mmHg or treatment with oral antihypertensive drugs. † eGFR was calculated with the use of the simplified Modification of Diet in Renal Disease formula. ‡ Myocardial rupture complicating ACS (free wall rupture, ventricular septal defect, acute mitral regurgitation). § Acute native or prosthetic valve incompetence secondary to endocarditis, aortic dissection or thrombosis. ¶ Severe anaemia defined as haemoglobin level between 4 g/dL and 8 g/dL. # Metabolic/hormonal derangements defined as thyroid dysfunction, adrenal dysfunction or pregnancy and peripartum-related abnormalities. ** Toxic substances (alcohol, recreational drugs), cardiodepressant and other treatments (non-steroidal anti-inflammatory drugs, corticosteroids, negative inotropic substances, cardiotoxic chemotherapeutics). †† Acute kidney failure defined according to AKIN network (stage ≥ 1: absolute increase of serum creatinine 1.5–2.0 times from baseline or ≥0.3 mg/dL (≥26.5 µmol/L)). ‡‡ Cardiogenic shock was defined as hypotension (systolic blood pressure < 90 mmHg) despite adequate filling status associated with clinical and biological markers of hypoperfusion. §§ Troponin I assay was performed in biochemistry central lab on multiparametric automate Access/DXi 800 Beckman, as BNP. ¶¶ Inotropic agents: dobutamine, dopamine, levosimendan. ## Vasopressors: norepinephrine or epinephrine. *** Mechanical circulatory support includes Impella® device and veno-arterial extracorporeal membrane oxygenation. ††† Medical treatment strategy or failure of revascularisation. ‡‡‡ Detection of glucose concentration < 54 mg/dL (or <3 mmol/L) among all measurements obtained in all patients at any time during hospitalisation. §§§ Detection of glucose concentration ≥ 180 mg/dL (or ≥10 mmol/L) among all measurements obtained in all patients at any time during hospitalisation.