Correct! Based upon the results of STRONG-HF, high-intensity care for initiation and rapid up-titration of oral HF therapies and close follow-up in the first 6 weeks after discharge for an acute HF hospitalization is recommended to reduce HF readmission or all-cause death.

Incorrect. Based upon the results of STRONG-HF, high-intensity care for initiation and rapid up-titration of oral HF therapies and close follow-up in the first 6 weeks after discharge for an acute HF hospitalization is recommended to reduce HF readmission or all-cause death.

Incorrect. Based upon the results of STRONG-HF, high-intensity care for initiation and rapid up-titration of oral HF therapies and close follow-up in the first 6 weeks after discharge for an acute HF hospitalization is recommended to reduce HF readmission or all-cause death.

Incorrect. In STRONG-HF, HFrEF, HFpEF, HFmrEF were evaluated. Therefore the recommended strategy applies to all types mentioned above.

Correct! LV (left ventricle) is symmetrically hypertrophic with AL but asymmetrically hypertrophic in TTR amyloidosis, giving the appearance of a sigmoid septum. TTR amyloidosis causes greater decline in LV systolic and diastolic function than AL amyloidosis. It also causes a greater increase in LV and RV masses.

Incorrect. It helps to differentiate amyloidosis from hypertensive heart disease and sarcoidosis. However, it cannot differentiate between TTR and AL amyloidosis.

Correct! Grade 2 to 3 uptake on 99mtechnetium-pyrophosphate (99mTcPYP) scintigraphy is typical for ATTR amyloidosis. On the other hand there is poor or no (grade 0 to 1) radioisotope uptake in AL amyloidosis.

Correct! Abnormal sFLC ratio or positive M protein on immunofixation suggests AL amyloidosis and a bone marrow biopsy should be performed.

Incorrect! Oxygen is recommended in patients with SpO2 <90% or PaO2 <60 mmHg to correct hypoxaemia.

Incorrect. Intubation is recommended for progressive respiratory failure persisting in spite of oxygen administration or non-invasive ventilation.

Correct! Non-invasive positive pressure ventilation should be considered in patients with respiratory distress (respiratory rate >25 breaths/min, SpO2 <90%) and started as soon as possible in order to decrease respiratory distress and reduce the rate of mechanical endotracheal intubation.

Incorrect.

Correct! Intravenous loop diuretics are a drug of choice for decongestion.

Correct! Combination of a loop diuretic with thiazide-type diuretic should be considered in patients with resistant oedema who do not respond to an increase in loop diuretic doses.

Incorrect. Inotropic agents are not recommended routinely, due to safety concerns, unless the patient has symptomatic hypotension and evidence of hypoperfusion.

Correct! Inotropic agents may be considered in patients with SBP <90 mmHg and evidence of hypoperfusion who do not respond to standard treatment, including fluid challenge, to improve peripheral perfusion and maintain end-organ function.

Incorrect. CRT is recommended for symptomatic patients with HF in sinus rhythm with a QRS duration of 130-149 ms and LBBB QRS morphology and with LVEF <35% despite OMT. (Class IIa) Several studies have shown that patients with left bundle branch block (LBBB) morphology are more likely to respond favourably to CRT, whereas there is less certainty about patients with non-LBBB morphology.

Incorrect. CRT is not recommended in patients with a QRS duration <130 ms who do not have an indication for pacing due to high degree AV block. (Class III)) The Echo-CRT trial and an IPD meta-analysis suggest possible harm from CRT when QRS duration is <130 ms.

Correct! CRT should be considered for symptomatic patients with HF in SR with a QRS duration >150 ms and non-LBBB QRS morphology and with LVEF <35% despite OMT (Class IIa) and is recommended in patient with LBBB QRS morphology (Class I).

Incorrect. Patients with HFrEF of an ischaemic aetiology have less improvement in LV function with CRT due to myocardial scar tissue, which is less likely to undergo favourable remodelling.

Incorrect. A vasopressor, preferably norepinephrine, may be considered in patients with cardiogenic shock to increase blood pressure and vital organ perfusion. Dopamine was compared with norepinephrine as a first-line vasopressor therapy in patients with shock and was associated with more arrhythmic events and with a greater mortality.

Correct! Thromboembolism prophylaxis (e.g. with LMWH) is recommended in patients not already anticoagulated and with no contraindication to anticoagulation, to reduce the risk of deep venous thrombosis and pulmonary embolism.

Incorrect. Routine use of opiates is not recommended, unless in selected patients with severe/intractable pain or anxiety.

Incorrect. thromboembolism prophylaxis (e.g. with LMWH) is recommended in patients not already anticoagulated and with no contraindication to anticoagulation, to reduce the risk of deep venous thrombosis and pulmonary embolism.

Correct! SGLT2 inhibitors are recommended in patients with T2DM at risk of CV events to reduce hospitalizations for HF, major CV events, end-stage renal disease, and CV death.

Incorrect. Thiazolidinediones (glitazones) are not recommended in patients with HF, as they increase the risk of HF worsening and HF hospitalization.

Incorrect. The DPP-4 inhibitor saxagliptin is not recommended in patients with HF. According to SAVOR-TIMI 53 the heart-failure-associated hospitalization rate increased in the saxagliptin-treated patients compared to the control group.

Incorrect. SGLT2 inhibitors are recommended in patients with T2DM at risk of CV events to reduce hospitalizations for HF, major CV events, end-stage renal disease, and CV death.

Correct! ECG is recommended in all patients for exclusion of ACS or arrhythmias. It should be done at admission, during hospitalization and pre-discharge.

Correct! Echocardiography is recommended in all patients. There might be findings of congestion, cardiac dysfunction or mechanical causes.

Correct! Serum troponine should be measured in all pateints at admission to rule out ACS.

Incorrect. Measurement of D-dimer concentration is recommended if pulmonary embolism is suspected.

Correct! Echocardiography remains the main non-invasive method in the diagnosis of patients with heart failure with preserved ejection fraction. HFpEF patients considered those with LVEF ≥50% and signs of diastolic dysfunction.

Correct! CMR is the best alternative imaging modality of the heart in patients with non-diagnostic echocardiographic examinations due to suboptimal image quality.

Correct! It is an algorithm for diagnosing HFpEF - HFA-PEFF, where P is a pre-test probability, E is a set of data from Echo and natriuretic peptides, F1-functional tests, in particular, diastolic stress test, F2-final conclusions on the aetiology of the pathological process.

Correct! Right heart catheterization may be considered in selected patients with HFpEF to confirm the diagnosis (e.g. restrictive cardiomyopathy).

Correct! SGLT2-inhibitors showed significant benefit on heart failure hospitalization rates and are now recommended in patients with HFpEF. Two randomized clinical trials (EMPEROR-Preserved and DELIVER) showed that the SGLT-2 inhibitors empaglifozin and dapaglifozin significantly reduce the primary composite endpoint of hospitalization for heart failure and cardiovascular death.

Incorrect. In the Paragon HF, the primary endpoint of total hospitalization due to heart failure or cardiovascular death was narrowly missed. However, not surprisingly in the adjusted rate ratio for primary endpoint by subgroups LVEF (below 57% median) displayed a significant reduction of RR (relative risk).

Correct! Both the preclinical data and the currently available clinical data with finerenone demonstrate a yet to be precisely defined therapeutic potential of this non-steroidal MRA in patients with HFpEF. Finally, this question will be answered in the ongoing FINEARTS-HF Study (Estimated Study Completion Date: June 19, 2024) to Evaluate the Efficacy and Safety of Finerenone on Morbidity & Mortality in Participants with Heart Failure and LV-Ejection Fraction ≥ 40%).

Correct! It is important to identify and treat the underlying risk factors, aetiology, and coexisting comorbidities in HFpEF (e.g. hypertension,CAD, amyloidosis, AF and valvular heart disease.

Incorrect. Patients with HFpEF are older and more often female in contrary to patients with HFrEF and HFmrEF. AF, CKD, and non-CV comorbidities are more common in these patients.

Incorrect. Ischemic etiology is much more common in HFrEF. The most prevalent comorbidities in HFpEF are hypertension, ischaemic heart disease, diabetes and atrial fibrillation.

Correct! Longitudinal follow-up studies have suggested that the prevalence of HFpEF is increasing and may reflect the ageing and greater comorbidities present in population in the developed world as well as an increased awareness of the diagnosis.

Incorrect. Patients with a history of overtly reduced LVEF (<40%), who later present with LVEF >50%, should be considered to have recovered HFrEF or ‘HF with improved LVEF’ (rather than HFpEF). Continued treatment for HFrEF is recommended in these patients.

Correct! According to STRONG-HF trial (significant reduction in HF hospitalization). Also post hoc secondary analysis from the STRONG-HF study demonstrated that higher achieved doses of HF GDMT medications were associated with better outcomes and greater improvement of quality of life, with the best results seen in patients treated with an average dose of 90% or more of maximally recommended doses. Therefore, when patients can tolerate higher doses of GDMT, all efforts should be made to rapidly uptitrate patients with AHF to optimal doses of the 3 and (likely) 4 pillars of HF medications, including RAS inhibitors, BBs, MRAs and SGLT2 inhibitors.

Correct! According to STRONG-HF trial (significant reduction in HF hospitalization). Also post hoc secondary analysis from the STRONG-HF study demonstrated that higher achieved doses of HF GDMT medications were associated with better outcomes and greater improvement of quality of life, with the best results seen in patients treated with an average dose of 90% or more of maximally recommended doses. Therefore, when patients can tolerate higher doses of GDMT, all efforts should be made to rapidly uptitrate patients with AHF to optimal doses of the 3 and (likely) 4 pillars of HF medications, including RAS inhibitors, BBs, MRAs and SGLT2 inhibitors.

Correct! According to STRONG-HF trial (significant reduction in HF hospitalization). Also post hoc secondary analysis from the STRONG-HF study demonstrated that higher achieved doses of HF GDMT medications were associated with better outcomes and greater improvement of quality of life, with the best results seen in patients treated with an average dose of 90% or more of maximally recommended doses. Therefore, when patients can tolerate higher doses of GDMT, all efforts should be made to rapidly uptitrate patients with AHF to optimal doses of the 3 and (likely) 4 pillars of HF medications, including RAS inhibitors, BBs, MRAs and SGLT2 inhibitors.

Correct! According to STRONG-HF trial (significant reduction in HF hospitalization). Also post hoc secondary analysis from the STRONG-HF study demonstrated that higher achieved doses of HF GDMT medications were associated with better outcomes and greater improvement of quality of life, with the best results seen in patients treated with an average dose of 90% or more of maximally recommended doses. Therefore, when patients can tolerate higher doses of GDMT, all efforts should be made to rapidly uptitrate patients with AHF to optimal doses of the 3 and (likely) 4 pillars of HF medications, including RAS inhibitors, BBs, MRAs and SGLT2 inhibitors.

Correct! NT-proBNP >125 (SR = sinus rhytm) or >365 (AF = atrial fibrilation) pg/mL, BNP >35 (SR) or >105 (AF) pg/mL. However up to 20% of patients with invasively proven HFpEF have NPs below diagnostic thresholds, particularly in the presence of obesity.

Correct! Left atrial dilation means >34 mL/m2 (SR) in the absence of AF or valve disease. LA enlargement reflects chronically elevated LV filling pressure (in the presence of AF, the threshold is >40 mL/m2 ).

Correct! Left ventricular hypertrophy without dilatation is characteristic for impaired diastolic function. Although the presence of concentric LV remodelling or hypertrophy is supportive for the diagnosis, the absence of LV hypertrophy does not exclude the diagnosis of HFpEF.

Correct. Sensitivity 78%, specificity 59% for the presence of HFpEF by invasive exercise testing, although reported accuracy has varied.

Correct! Follow-up is recommend at intervals no longer than 6 months to check symptoms, heart rate and rhythm, blood pressure, full blood count, electrolytes, and renal function.

Incorrect. An ECG should be done annually to detect QRS prolongation as such patients may become candidates for cardiac resynchronization therapy. Furthermore, it may identify conduction disturbances and AF.

Incorrect. Serial echocardiography is generally not necessary, although an echocardiogram should be repeated if there has been a deterioration in clinical status.

Incorrect. Current evidence does not support routine measurement of BNP or NT-proBNP to guide titration of therapy. However they are undoubtedly good prognostic markers.

Incorrect. A severely reduced LVEF is common but not required for a diagnosis of advanced HF as it may develop in patients with HFpEF as well.

Incorrect. Extra-cardiac organ dysfunction due to HF (e.g. cardiac cachexia, liver or kidney dysfunction) or type II pulmonary hypertension may be present, but are not required for the definition of advanced HF.

Correct! Severe and persistent symptoms of heart failure (NYHA class III/IV) are criteria for the definition of an advanced heart failure.

Correct! Episodes of pulmonary or systemic congestion requiring high-dose i.v. diuretics are criteria for the definition of an advanced heart failure.

Profile 1. is critical cardiogenic shock Patient with life-threatening hypotension despite rapidly escalating inotropic support, critical organ hypoperfusion, often confirmed by worsening acidosis and/or lactate levels. “Crash and burn.” Definitive intervention needed within hours.

Profile 2. is progressive decline. Patient with declining function despite i.v. inotropic support, may be manifest by worsening renal function, nutritional depletion, inability to restore volume balance. “Sliding on inotropes.” Also describes declining status in patients unable to tolerate inotropic therapy. Definitive intervention needed within few days.

Profile 3. is stable on inotrope or inotrope-dependent. Patient with stable blood pressure, organ function, nutrition, and symptoms on continuous i.v. inotropic support (or a temporary circulatory support device or both) but demonstrating repeated failure to wean from support due to recurrent symptomatic hypotension or renal dysfunction. “Dependent stability.” Definitive intervention elective over a period of weeks to few months.

Profile 4. is Frequent Flyer. Patient can be stabilized close to normal volume status but experiences daily symptoms of congestion at rest or during activities of daily living. Doses of diuretics generally fluctuate at very high levels. More intensive management and surveillance strategies should be considered, which may in some cases reveal poor compliance that would compromise outcomes with any therapy. Some patients may shuttle between 4 and 5. Definitive intervention elective over a period of weeks to few months.

Correct! BTD = Use of short-term MCS (ECMO or Impella) in patients with cardiogenic shock until haemodynamics and end-organ perfusion are stabilized, contraindications for long-term MCS are excluded (brain damage after resuscitation). Additional therapeutic options including long-term VAD (ventricular assist device) therapy or heart transplant can be evaluated.

Correct! BTR = Use of MCS (short-term or long-term) to keep a patient alive until cardiac function recovers sufficiently to remove MCS.

Correct! BTB = Use of short-term MCS (ECMO or Impella) in patients with cardiogenic shock until haemodynamics and end-organ perfusion are stabilized, contraindications for long-term MCS are excluded (brain damage after resuscitation). Additional therapeutic options including long-term VAD (ventricular assist device) therapy or heart transplant can be evaluated.

Incorrect. DT = Long-term use of MCS (LVAD) as an alternative to transplantation in patients with end-stage HF ineligible for transplantation.

Incorrect. Active infection is a relative contraindication to transplant but in some cases of infected LVADs it may actually be an indication.

Incorrect. Elderly age is not an absolute contraindication. Although patients aged <65 years might be more appropriate candidates due to their overall life expectancy, most programmes accept patients up to 70 years of age, and biological age as well as chronological age must be taken into account.

Correct! In these patients LVAD should be considered to reverse elevated pulmonary vascular resistance with subsequent re-evaluation to establish candidacy.

Correct! Weight loss is recommended to achieve a BMI <35 kg/m2.

Correct! EuroHeart Failure Survey II (EHFS II): a survey on hospitalized acute heart failure patients. In-hospital mortality ranges from 4% to 10%.

Incorrect. There is lower post-discharge mortality. Post-discharge 1-year mortality can ranges from 25 to 30%.

Incorrect. There is lower rehospitalization rates.

Incorrect. AHF may be the first manifestation of HF (new onset) but is more frequently due to an acute decompensation of chronic HF.

Incorrect. Long-term MCS should be considered in patients with INTERMACS profiles 2 to 4 and also in patients with INTERMACS profile 5 and 6, when they have high-risk characteristics. Short-term MCS should be used in patients with INTERMACS profiles 1 or 2.

Incorrect. Impella is used as a short-term MCS. Impella comes in various sizes and can deliver 2.5–5.5 l/min of flow, depending on the device. Impella 5.5 is now approved for up to 30 days of support.

Correct. Long-term MCS is indicated in selected patients when medical therapy is insufficient or when short-term MCS has not led to cardiac recovery or clinical improvement. They are used to prolong life and improve quality of life, or to keep the patient alive until transplantation (bridge to transplantation, BTT) or to reverse contraindications to heart transplantation (bridge to candidacy, BTC), or as destination therapy (DT).

Correct! Stable psychosocial background includes demonstrated understanding of the technology and patient living in the same household with a caregiver that will help the patient are mandatory in patients indicated for LVAD.

Incorrect. There was a greater relief of dyspnoea, change in weight and net fluid loss in the higher-dose regimen. However high diuretic doses may cause greater neurohormonal activation and electrolyte abnormalities and are often associated with poorer outcomes.

Correct! Based on these observations, it may be appropriate, when starting i.v. diuretic treatment, to use low doses, to assess the diuretic response and increase the dose when that is insufficient.

Incorrect. We use this dose if the patient was not taking oral diuretics prior to admission for AHF. The dose that should be used for a patient who has taken diuretics prior to admission is 1-2 times his/her daily oral dose.

Incorrect. Daily single bolus administrations are discouraged because of the possibility of post-dosing sodium retention. Furosemide can be given as 2-3 daily boluses or as a continuous infusion.

Incorrect. Epinephrine was associated with higher incidence of refractory shock, higher heart rate and also lactic acidosis. There is three-fold increase in the risk of death with epinephrine, compared with norepinephrine.

Correct! Studies, though with limitations, support the use of norepinephrine as first choice, compared with dopamine or epinephrine.

Incorrect. Dopamine compared to norepinephrine was associated with more arrhythmic events and with a greater mortality in patients with cardiogenic shock.

Incorrect, studies, though with limitations, support the use of norepinephrine as first choice, compared with dopamine or epinephrine.

Correct! The benefits of SGLT-2i are consistent across many CKD with coexistent HF subgroups regardless of the T2DM status. In addition, SGLT-2i reduce new-onset anemia and hyperkalemia in patients with CKD and are safe and generally well tolerated.

Correct! Finerenone exhibited significant renoprotective and cardioprotective effects in two recent clinical trials that recruited patients with CKD and type 2 diabetes mellitus. (FIDELIO-DKD, FIGARO-DKD).

Incorrect. In patients with TD2M and CKD, finerenone is recommended.

Incorrect. Spironolactone has been shown to be effective in reducing LVH and can be safely used, while currently, the drug with the greatest promise in reducing cardiovascular risk in patients with CKD is finerenone.

Correct! Beta-blockers are the mainstay of therapy in patients with HFrEF and coronary artery disease because of their prognostic benefit.

Correct. Ivabradine should be considered as an alternative to beta-blockers (when contraindicated) or as additional anti-anginal therapy in patients in SR whose heart rate is >70 b.p.m.

Correct! Trimetazidine seems to have additive effects, such as improvement of LV function and exercise capacity, in patients with HFrEF and CCS already on beta-blockers. It may be considered in patients with HF and angina despite beta-blocker and/or ivabradine.

Incorrect. Verapamil and diltiazem increase HF-related events in patients with HFrEF and are contraindicated.

Incorrect. Every effort should be made to reach target doses of evidence-based medications in HFrEF patients, despite slight hypotension.

Correct! In HFpEF patients with left ventricular hypertrophy and limited preload reserve, hypotension should be avoided.

Incorrect. In HFpEF patients with LVH and limited preload reserve, hypotension should be avoided.

Incorrect. In HFpEF patients with LVH and limited preload reserve, hypotension should be avoided.

Correct! It is well accepted that angiotensin-converting enzyme (ACE) inhibitors are contraindicated during the second and third trimesters of pregnancy because of an increased risk of fetal renal damage. They should be stopped prior to conception with close clinical and echocardiographic monitoring.

Incorrect. Beta-blockers should be continued and switched to beta-1-selective blockers. They are used frequently for the treatment of several cardiovascular conditions during pregnancy. Large, retrospective studies show no association between the use of beta-blockers and major congenital abnormalities. However beta-blockers are associated with intrauterine growth restriction, increased risk of preterm birth, and neonatal bradycardia and hypoglycemia.

Correct! Spironolactone might lead to undervirilization of male infants due to the anti-androgenic effects. Although data in the literature are very limited, treatment with spironolactone is not recommended.

Correct! SGLT2 inhibitors are contraindicated and should be stopped prior to conception with close clinical and echocardiographic monitoring. They can cause dilation of the renal pelvis and tubules, congenital anomalies and an increased rate of miscarriages.

Correct! Signs we can find on echogardiography are new structural or function abnormalities, regional wall motion abnormalities or global ventricular dysfunction without ventricular dilation or with, generally mild, dilation, increased wall thickness due to myocardial oedema, pericardial effusion, intracardiac thrombi, not explained by other conditions (e.g., coronary artery disease, ACS or valvular heart disease).

Correct! CMR in myocarditis can show oedema, inflammation and fibrosis detection, quantification and localization through T1 and T2 mapping, extracellular volume assessment and LGE.

Correct! ECG findings in myocarditis are new and dynamic ST-T abnormalities, including pseudo-infarct ST segment elevation, atrial or ventricular arrhythmias, AV blocks, QRS abnormalities.

Incorrect. EMB is an additional diagnostic test. It's indicated in progressive or persistent severe cardiac dysfunction and/or life-threatening ventricular arrhythmias and/or Mobitz type 2 second-degree or higher AV block with lack of short-term (<1-2 weeks) expected response to usual medical treatment. The aim is to identify aetiology and to indicate specific treatment (e.g. giant cell myocarditis, eosinophilic myocarditis, cardiac sarcoidosis, systemic inflammatory disorders).

Incorrect. HF therapy should be started if left ventricle systolic dysfunction is present at presentation and should be continued for at least 6 months upon complete functional recovery (EF >50%).

Incorrect. Immunosuppression is not advised on a routine basis in acute myocarditis without clinical or endomyocardial biopsy based evidence of auto-immune disease.

Correct. Intense sporting activities should be avoided as long as symptoms, cardiac enzymes elevated or ECG/imaging abnormalities are present and last for at least 6 months since complete recovery.

Correct. Yearly follow-up for at least 4 years, with an ECG and echocardiography, is needed as acute myocarditis may lead to dilated cardiomyopathy in up to 20% of cases.

Correct. Although, there is a lack of controlled studies showing that diuretics are of benefit in acute pulmonary oedema, diuretics are indicated for patients with evidence of fluid overload.

Correct! Higher doses cause arteriolar dilation, resulting in reduced afterload and blood pressure. Specifically in the coronary arteries, this dilation results in an increased coronary blood flow. These actions collectively improve oxygenation and reduce the workload of the heart. However they should not be given if the systolic blood pressure is less than 90 mmHg or the patient has severe aortic stenosis, as these patients are preload dependent.

Correct! NIV is now the recommended first-line method of ventilator support in cardiogenic pulmonary oedema. Use of non-invasive positive airway pressure can decrease the systemic venous return and the left ventricular (LV) afterload, thus reducing LV filling pressure and limiting pulmonary edema. In these patients, either non-invasive ventilation (NIV) or continuous positive airway pressure (CPAP) can improve vital signs and physiological parameters, decreasing the need for endotracheal intubation (ETI) and hospital mortality when compared to conventional oxygen therapy.

Incorrect. Morphine is no longer recommended for routine use in acute pulmonary oedema. It has been associated with adverse events such as significantly increased rates of mechanical ventilation, intensive care admissions and mortality. However it may be beneficial if there is ongoing chest pain resistant to nitrates. Low doses of morphine (1–2.5 mg) can be useful to facilitate the tolerance of non-invasive ventilation but the patient needs to be monitored for sedation.

Incorrect. A small randomized controlled trial conducted in self-identified black patients showed that an addition of the combination of hydralazine and isosorbide dinitrate to conventional therapy (an ACE-I, a beta-blocker, and an MRA) reduced mortality and HF hospitalizations in patients with HFrEF. These results are difficult to translate to patients of other racial or ethnic origins.

Correct! ARBs are now recommended for patients who cannot tolerate ACE-I or ARNI because of serious side effects. Candesartan in the CHARM-Alternative study reduced CV deaths and HF hospitalizations in patients who were not receiving an ACE-I due to previous intolerance. Valsartan, in addition to usual therapy, including ACE-I, reduced HF hospitalizations in the Val-HeFT trial. However, no ARB has reduced all-cause mortality in any trial.

Incorrect. ARBs are now recommended for patients who cannot tolerate ACE-I or ARNI because of serious side effects. Candesartan in the CHARM-Alternative study reduced CV deaths and HF hospitalizations in patients who were not receiving an ACE-I due to previous intolerance. Valsartan, in addition to usual therapy, including ACE-I, reduced HF hospitalizations in the Val-HeFT trial. However, no ARB has reduced all-cause mortality in any trial.

Incorrect. ARBs are now recommended for patients who cannot tolerate ACE-I or ARNI because of serious side effects. Candesartan in the CHARM-Alternative study reduced CV deaths and HF hospitalizations in patients who were not receiving an ACE-I due to previous intolerance. Valsartan, in addition to usual therapy, including ACE-I, reduced HF hospitalizations in the Val-HeFT trial. However, no ARB has reduced all-cause mortality in any trial.

Correct! For patients in NYHA class III, a beta-blocker, usually given orally, is safe and therefore is recommended as firstline treatment to control ventricular rate.

Incorrect. The use of nondihydropyridine calcium channel blockers (NDCCBs) to achieve rate control in atrial fibrillation with the rapid ventricular rate (AF RVR) is not recommended in patients with comorbid heart failure with reduced ejection fraction (HFrEF) due to the concern for further blunting of contractility.

Incorrect. Digoxin may be useful for the treatment of patients with HFrEF and AF with rapid ventricular rate, when other therapeutic options cannot be pursued.

Incorrect. In cases of a clear association between paroxysmal or persistent AF and worsening of HF symptoms, which persist despite medical therapy, catheter ablation should be considered for the prevention or treatment of AF.

Correct! Those are indication criteria for ICD implantation.

Incorrect. Current guidelines do not recommend ICDs for most NYHA class IV heart failure patients, as the risk of cardiac decompensation and pump failure outweigh those of sudden cardiac death.

Incorrect. Patients need to be expected to survive for >1 year with good functional status.

Incorrect. ICD implantation is not recommended within 40 days of a MI as implantation at this time does not improve prognosis.

Incorrect. Cough is a very common side effect of ACEi.

Correct. Serious urinary tract infections, including urosepsis and pyelonephritis, are associated with SGLT2 inhibitors. SGLT2 inhibitors inhibit glucose reabsorption in the proximal tubules, leading to glycosuria and an increased risk of UTI. Meta-analysis of 52 RCTs showed that dapagliflozin had a dose-response relationship with UTI.

Incorrect. The risk of hypoglycemia is increased with SGLT2 concomitant administration of insulin secretagogues such as sulfonylureas or insulin. Physicians should reduce the dose of the insulin secretagogue or insulin when combined with SGLT2 inhibitors.

Correct. SGLT-2 inhibitors are associated with an almost 3-fold increased risk for diabetic ketoacidosis. The risk for diabetic ketoacidosis is highest for canagliflozin, followed by empagliflozin and dapagliflozin.

Incorrect. Both carboxymaltose and ferric derisomaltose are recommended.

Incorrect. Both carboxymaltose and ferric derisomaltose are recommended.

Correct! Studies showed decrease in the number of hospitalizations, significant NYHA class improvements and quality of life improvement in patients treated with i.v. ferric carboxymaltose (The AFFIRM-AHF trial). For a broad range of patients with heart failure, reduced left ventricular ejection fraction and iron deficiency, intravenous ferric derisomaltose administration was associated with a lower risk of hospital admissions for heart failure and cardiovascular death (IRONMAN study).

Incorrect. Studies showed decrease in the number of hospitalizations, significant NYHA class improvements and quality of life improvement in patients treated with i.v. ferric carboxymaltose (The AFFIRM-AHF trial). For a broad range of patients with heart failure, reduced left ventricular ejection fraction and iron deficiency, intravenous ferric derisomaltose administration was associated with a lower risk of hospital admissions for heart failure and cardiovascular death (IRONMAN study).

Incorrect. BNP values are lower in obese patiens. A number of hypotheses have been put forth in an attempt to explain the inverse relationship between obesity and circulating BNP levels. One of them is higher glomerular filtration rates associated with obesity, which then leads to a decrease in BNP levels. Adipocytes are also known to highly express natriuretic peptide clearance receptors-C (NPR-C), causing some to speculate that this is the basis for low serum BNP levels associated with obesity.

Correct! Chronic anemia is known to result in an increased venous return and increased cardiac work which may lead to LVH and subsequent cardiac enlargement. Over time functional changes occur, with impaired LV ventricular relaxation and compliance. In the presence of LVH and anemia, there is also a reduction in the level of coronary vasodilator reserve resulting in myocardial ischemia. An ischemic heart is more sensitive to even smaller drops in hemoglobin, yielding worsening of cardiac function. It is possible that level of BNP is the result of subclinical ventricular dysfunction.

Incorrect. Pregnancy does not affect BNP levels.

Correct! The pathophysiological processes leading to elevated BNP levels in COPD are not well understood. In patients with severe COPD, hypoxia and pulmonary vasoconstriction can lead to pulmonary hypertension and right ventricular dysfunction, which then leads to elevation in BNP levels.

Correct!. In addition to inhibiting the RAAS axis, ARNIs also function as inhibitors of neprilysin, which is responsible for the degradation of BNP. When this enzyme is inactivated, the lifespan of BNP is prolonged and the concentration of NT-proBNP decreases.

Incorrect. In addition to inhibiting the RAAS axis, ARNIs also function as inhibitors of neprilysin, which is responsible for the degradation of BNP. When this enzyme is inactivated, the lifespan of BNP is prolonged and the concentration of NT-proBNP decreases.

Correct! This results mainly from the RAAS inhibition.

Incorrect. In addition to inhibiting the RAAS axis, ARNIs also function as inhibitors of neprilysin, which is responsible for the degradation of BNP. When this enzyme is inactivated, the lifespan of BNP is prolonged and the concentration of NT-proBNP decreases.

Correct! There are 3 beta-blockers with proven reduced mortality benefit - Bisoprolol (CIBIS II), Carvedilol (COPRNICUS) and Metoprolol (MERIT HF).

Correct! ARNIs improve the survival rate of heart failure patients by inhibition of neprilysin and RAAS which leads to an increase in ANP (atrial natriuretic peptide) and BNP (brain natriuretic peptide) levels, which in turn has beneficial effects on preload, inflammation, and fibrosis.

Correct! DAPA-HF trial was the first study that evaluated the efficacy of an SGLT-2 inhibitor in patients with HFrEF. Dapagliflozin was found to significantly reduce the primary composite outcome of cardiovascular death, HF hospitalizations, and urgent HF visits compared to placebo. EMPEROR-Reduced trial evaluated the efficacy of empagliflozin, which significantly reduced the composite outcome of cardiovascular death and HF hospitalizations compared to placebo with a relative risk reduction of 21%.

Incorrect. Loop diuretics are recommended in patients with HFrEF and signs/symptoms of congestion. However, it is a symptomatic treatment only and does not reduce morbidity or mortality.

Correct! According to CIBIS II 1999 34% relative risk reduction in all-cause mortality was noted in patients LVEF < 35% and NYHA class III-IV treated with bisoprolol.

Correct! According to COPERNICUS 2001 31% relative risk reduction in all-cause mortality was noted in patients LVEF < 25% and NYHA class III-IV treated with carvedilol.

Correct! According to MERIT HF 1999 34% relative risk reduction in all-cause mortality was noted in patients LVEF < 35% and NYHA class II-IV treated with metorpolol.

Incorrect. Although, nebivolol is one of four recommended beta-blockers used for patients with HFrEF, no study has ever documented a significant reduction in mortality associated with nebivolol administration.

Incorrect. Vericiguat is recommended as an add-on therapy in symptomatic patients with HFrEF despite optimal therapy, This was proven in the VICTORIA study where the incidence of primary endpoint (death from CV causes or hospitalization for HF) was lower among those who received vericiguat than among those who received placebo.

Incorrect. Vericiguat is recommended as an add-on therapy in symptomatic patients with HFrEF despite optimal therapy, This was proven in the VICTORIA study, where the incidence of primary endpoint (death from CV causes or hospitalization for HF) was lower among those who received vericiguat than among those who received placebo.

Correct! Vericiguat may be considered in patients in NYHA class II-IV who have had worsening HF despite treatment with an ACE-I(or ARNI), a beta-blocker and an MRA to reduce the risk of CV mortality or HF hospitalization (Class IIb). This was proven in the VICTORIA study, where the incidence of primary endpoint (death from CV causes or hospitalization for HF) was lower among those who received vericiguat than among those who received placebo.

Incorrect. Vericiguat is recommended as an add-on therapy in symptomatic patients with HFrEF despite optimal therapy, This was proven in the VICTORIA study, where the incidence of primary endpoint (death from CV causes or hospitalization for HF) was lower among those who received vericiguat than among those who received placebo.

Incorrect. Ivabradine should be considered in patients with HFrEF and a heart rate ≥70 bpm despite optimal medical therapy. Ivabradine reduced the combined endpoint of CV mortality and HF hospitalization in patients with symptomatic HFrEF with an LVEF ≤35%, with HF hospitalization in recent 12 months, in sinus rhythm (SR) and with a heart rate ≥70 b.p.m. who were on evidence-based therapy including an ACE-I (or ARB), a beta-blocker, and an MRA.

Correct. Ivabradine should be considered in patients with HFrEF and a heart rate ≥70 bpm despite optimal medical therapy (Class IIa). Ivabradine reduced the combined endpoint of CV mortality and HF hospitalization in patients with symptomatic HFrEF with an LVEF ≤35%, with HF hospitalization in recent 12 months, in sinus rhythm (SR) and with a heart rate ≥70 b.p.m. who were on evidence-based therapy including an ACE-I (or ARB), a beta-blocker, and an MRA.

Incorrect. Ivabradine should be considered in patients with HFrEF and a heart rate ≥70 bpm despite optimal medical therapy. Ivabradine reduced the combined endpoint of CV mortality and HF hospitalization in patients with symptomatic HFrEF with an LVEF ≤35%, with HF hospitalization in recent 12 months, in sinus rhythm (SR) and with a heart rate ≥70 b.p.m. who were on evidence-based therapy including an ACE-I (or ARB), a beta-blocker, and an MRA.

Incorrect. Ivabradine should be considered in patients with HFrEF and a heart rate ≥70 bpm despite optimal medical therapy. Ivabradine reduced the combined endpoint of CV mortality and HF hospitalization in patients with symptomatic HFrEF with an LVEF ≤35%, with HF hospitalization in recent 12 months, in sinus rhythm (SR) and with a heart rate ≥70 b.p.m. who were on evidence-based therapy including an ACE-I (or ARB), a beta-blocker, and an MRA.

Incorrect. Influenza and pneumococcal vaccination, as well as COVID-19 vaccination, when available, should be considered in patients with HF. (Class IIa) Infective disorders may worsen HF symptoms and be a precipitant factor for acute heart failure. Severe sepsis and pneumonia can cause myocardial injury and depress cardiac function leading to cardiac dysfunction and HF and this risk is greater in patients with a history of HF.

Incorrect. Influenza and pneumococcal vaccination, as well as COVID-19 vaccination, when available, should be considered in patients with HF. (Class IIa) Infective disorders may worsen HF symptoms and be a precipitant factor for acute heart failure. Severe sepsis and pneumonia can cause myocardial injury and depress cardiac function leading to cardiac dysfunction and HF and this risk is greater in patients with a history of HF.

Correct! Influenza and pneumococcal vaccination, as well as COVID-19 vaccination, when available, should be considered in patients with HF. (Class IIa) Infective disorders may worsen HF symptoms and be a precipitant factor for acute heart failure. Severe sepsis and pneumonia can cause myocardial injury and depress cardiac function leading to cardiac dysfunction and HF and this risk is greater in patients with a history of HF.

Correct! Influenza and pneumococcal vaccination, as well as COVID-19 vaccination, when available, should be considered in patients with HF. (Class IIa) Infective disorders may worsen HF symptoms and be a precipitant factor for acute heart failure. Severe sepsis and pneumonia can cause myocardial injury and depress cardiac function leading to cardiac dysfunction and HF and this risk is greater in patients with a history of HF.

Incorrect. Diagnostic tests include ECG, echocardiography, and additional investigations such as chest X-ray and lung ultrasound, especially when NP testing is unavailable. Plasma NP levels (BNP, NT-proBNP, or MR-proANP) should be measured if the diagnosis is uncertain and a point-of-care assay is available. Normal NP concentrations make AHF diagnosis unlikely, with cut-offs for acute HF set at BNP <100 pg/mL, NT-proBNP <300 pg/mL, and MR-proANP <120 pg/mL. However, elevated NP values are associated with various cardiac and non-cardiac conditions

Correct. Diagnostic tests include ECG, echocardiography, and additional investigations such as chest X-ray and lung ultrasound, especially when NP testing is unavailable. Plasma NP levels (BNP, NT-proBNP, or MR-proANP) should be measured if the diagnosis is uncertain and a point-of-care assay is available. Normal NP concentrations make AHF diagnosis unlikely, with cut-offs for acute HF set at BNP <100 pg/mL, NT-proBNP <300 pg/mL, and MR-proANP <120 pg/mL. However, elevated NP values are associated with various cardiac and non-cardiac conditions.

Incorrect. Diagnostic tests include ECG, echocardiography, and additional investigations such as chest X-ray and lung ultrasound, especially when NP testing is unavailable. Plasma NP levels (BNP, NT-proBNP, or MR-proANP) should be measured if the diagnosis is uncertain and a point-of-care assay is available. Normal NP concentrations make AHF diagnosis unlikely, with cut-offs for acute HF set at BNP <100 pg/mL, NT-proBNP <300 pg/mL, and MR-proANP <120 pg/mL. However, elevated NP values are associated with various cardiac and non-cardiac conditions

Incorrect. Diagnostic tests include ECG, echocardiography, and additional investigations such as chest X-ray and lung ultrasound, especially when NP testing is unavailable. Plasma NP levels (BNP, NT-proBNP, or MR-proANP) should be measured if the diagnosis is uncertain and a point-of-care assay is available. Normal NP concentrations make AHF diagnosis unlikely, with cut-offs for acute HF set at BNP <100 pg/mL, NT-proBNP <300 pg/mL, and MR-proANP <120 pg/mL. However, elevated NP values are associated with various cardiac and non-cardiac conditions

Incorrect. Spot urine sodium content should be evaluated after 2 or 6 hours of diuretic therapy. This method allows clinicians to promptly assess the effectiveness of diuretics. A satisfactory diuretic response is indicated by a urine sodium content greater than 50–70 mEq/L at 2 hours or 6 hours after diuretic administration. Urine output should be measured (urine output ≥ 100-150 mL/h after 6h is a marker of an effective diuretic therapy.

Incorrect. Spot urine sodium content should be evaluated after 2 or 6 hours of diuretic therapy. This method allows clinicians to promptly assess the effectiveness of diuretics. A satisfactory diuretic response is indicated by a urine sodium content greater than 50–70 mEq/L at 2 hours or 6 hours after diuretic administration. Urine output should be measured (urine output ≥ 100-150 mL/h after 6h is a marker of an effective diuretic therapy.

Incorrect. Spot urine sodium content should be evaluated after 2 or 6 hours of diuretic therapy. This method allows clinicians to promptly assess the effectiveness of diuretics. A satisfactory diuretic response is indicated by a urine sodium content greater than 50–70 mEq/L at 2 hours or 6 hours after diuretic administration. Urine output should be measured. (Urine output ≥ 100-150 mL/h after 6h is a marker of an effective diuretic therapy.)

Correct! Spot urine sodium content should be evaluated after 2 or 6 hours of diuretic therapy. This method allows clinicians to promptly assess the effectiveness of diuretics. A satisfactory diuretic response is indicated by a urine sodium content greater than 50–70 mEq/L at 2 hours or 6 hours after diuretic administration. Urine output should be measured. (Urine output ≥ 100-150 mL/h after 6h is a marker of an effective diuretic therapy.)

Correct! Studies showed decrease in the number of hospitalizations, significant NYHA class improvements and quality of life improvement in patients treated with i.v. ferric carboxymaltose.

Incorrect. Current clinical trials of erythropoiesis-stimulating agents have failed to provide convincing evidence of decreased morbidity and mortality or long-term effects, with an increased risk of administration due to the high incidence of thromboembolic complications.

Correct! All patients with HF should be periodically screened for anaemia and iron deficiency with a full blood count, serum ferritin concentration, and Transferrin saturation (TSAT).

Incorrect. In patients with heart failure with low ejection fraction (LVEF), it is recommended that iron deficiency should be treated by prescribing iron compounds with parenteral administration, as oral iron therapy is ineffective for replenishing iron stores.

Correct! LV wall thickness greater than 12 mm in the absence of hypertension should be evaluated as suspicious of CA.

Incorrect. This would rather be a sign of hypertrophic cardiomyopathy.

Correct! Amyloid infiltration of the myocardium leads to lower voltage.

Incorrect. The left ventricle is not dilated; rather, the ventricular dimensions are usually smaller than normal. On the contrary biatrial dilation is common.

Correct! EMB is the gold standard for the diagnosis of Transthyretin cardiac amyloidosis (TTR-CA) with nearly 100% sensitivity and specificity if specimens are collected from >4 multiple sites and tested for amyloid deposits by Congo red staining. Biopsy is not needed with a grade 2–3 positivity of scintigraphy with SPECT.

Correct! Technetium-labelled 99mTc-PYP or DPD or HMDP scintigraphy with planar and SPECT imaging has a specificity and positive predictive value for TTR-CA of up to 100%.

Correct! Key test in diagnosing cardiac amyloidosis. However, it cannot differentiate between Transthyretin (TTR) and Light chain immunoglobulin (AL) amyloidosis. Characteristic findings include restrictive morphology and diastolic dysfunction with disproportionate bi-atrial enlargement and increased myocardial mass and thickening.

Correct! Genotyping is important in patients with ATTR amyloidosis. More than 120 gene variants have been identified to cause cardiac amyloidosis. The two most common variants are Thr60Ala and Val122lle. Genotyping is essential to predict treatment response and prognosis. The type of variants depends on geographical location and ethnic variation.

Correct! MRA and loop diuretics remain the vital therapy options for heart failure management in cardiac amyloidosis. Hovewer orthostatic hypotension may cause intolerance. Peripheral vasoconstrictors such as midodrine can be used to maintain blood pressure while allowing diuresis to relieve congestion.

Incorrect. CCB should be avoided as they may cause severe hypotension and fatigue, or form complexes with amyloid.

Correct! Tafamidis reduced all-cause mortality and CV hospitalizations in cardiac or non-cardiac biopsy-proven hereditary and wtTTR-CA, mainly in those patients with NYHA class I and II at baseline. Functional improvement occurred within 6 months, whereas the decrease in mortality took nearly 2 years to occur.

Incorrect. Beta-blockers are poorly tolerated. Moreover profound hypotension on initiation of low doses of beta-blockers should raise suspicion for the possibility of underlying cardiac amyloidosis. ACE-I, ARBs, or ARNI may not be tolerated because of hypotension as well, and their place in CA treatment is unsettled.

Incorrect! Amyloid light chain amyloidosis (also known as Primary amyloidosis) is caused by the deposition of AL fibrils produced by abnormal plasma cells in patients with plasma cell dyscrasia such as multiple myeloma. It is second most common type of CA with the annual incidence of 1 per 100 000.

Correct! Wild transthyretin amyloidosis (also called Senile systemic) is caused by age-related amyloid deposition, which is made from normal TTR (transport-thyroxine-and-retinol) protein. This is the most prevalent type of cardiac amyloidosis. At least 10 to 15% of patients aged >65 years with heart failure with preserved ejection fraction may have cardiac amyloidosis.

Incorrect. Familial amyloidosis is caused by mutant TTR. With more than 100 TTR genes responsible for the disease, the exact prevalence of familial (hereditary) amyloidosis is unknown.

Incorrect. Isolated atrial amyloidosis is caused by the deposition of amyloid made from the atrial natriuretic peptide. Wild transthyretin amyloidosis is the most common etiological type of cardiac amyloidosis.