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Mitochondrial dysfunction can also lead to CMiPD development. This happens
because of excessive mitophagy causing an imbalance between mitophagy and
mitochondrial biogenesis. As a result, myocardial cells are destructed more
intensively [109].
It has been established that ketone metabolism can be an alternative to the
energy supply of the heart muscle [110]. The concentrations of circulating ketone
bodies increase in HF and they enter the cell as an insulin-independent energy
substrate. The appearance of ketone enzymes in a hypertrophied and damaged
heart leads to energy consumption for the oxidation of ketones with insufficient
possibilities for oxidation of fatty acids [111]. The presence of DM contributes to the
development of myocardial dysfunction and CHF due to the development and
maintenance of endothelial dysfunction, dyslipidemia, hypercoagulation, and the
direct effect of hyperglycemia on myocardial function and morphology [112]. At
the same time, in HF, as a result of organ hypoperfusion and hyperactivation of
neurohumoral systems (decrease in glucose consumption by muscle tissue, increased
gluconeogenesis in the liver, contra-insular effects of catecholaminemia), blood
glucose levels increase.
Thus, the development of HF in DM is due to the progression of atherosclerosis
with subsequent progression of myocardial ischemia and immediate myocardial
damage as a result of prolonged hyperglycemia. Myocardial damage against the
background of hyperglycemia is mediated by microangiopathy, impaired calcium
transport, and fatty acid metabolism. The presence of DM increases the risk of developing HF compared with that in the general population, and there is a significantly
higher mortality among DM patients with HF. In addition, an increased risk of developing HF was found in individuals with elevated values of morning glycemia even in
the absence of DM. Patients with HF have high insulin resistance and an increased risk
of developing DM [113].
6. Screening and diagnosing HF in people with diabetes
6.1 Electrocardiography (ECG)
According to the 2021 ESC guidelines’ recommendations, when patients’ symptoms signal the presence of acute or chronic HF, ECG is one of the measures used to
evaluate their condition [91]. If acute HF is detected, it is recommended to produce an
ECG when patients are admitted to the hospital, during their stay, and before they are
discharged [91]. Performing electrocardiography is mainly a step toward HF detection, such as changes in the ECG show higher chances of HF in patients and vice versa:
HF is not plausible when ECG is normal [91]. Moreover, by looking at the ECG, it is
possible to learn about the causes of HF and how to proceed with future treatment
[91]. Based on the 2019 ESC-EASD recommendations, ECG is also proposed for
“patients with diabetes who have been diagnosed with hypertension” [114].
6.2 Echocardiography
A cardiac injury manifests itself as structural changes and echocardiography is the
most effective and non-invasive measure to detect those changes [115], assessing
systolic and diastolic dysfunction [116]. Echocardiography is recommended by the
2021 ESC guidelines [91] and the 2019 ESC-EASD recommendations as the
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first-choice
since
symptoms
tional
but
it
hypertrophy
after
without
the
establishment of reference values for comparing subjects of various body sizes
[118].
43–95
Assessment of biomarkers
6.3
tool for structural and functional evaluation of the heart of diabetic people
it
can detect higher LV mass (LVM) and/or diastolic dysfunction when no
of HF
are present [114]. It is widely known that LVM is directly propor-
with common risk factors for T2D such as age, obesity, and dyslipidemia [117],
also relies on gender and body size [118]. It is worth mentioning that, LV
is a
common anomaly seen in asymptomatic T2D patients, such that even
omitting silent coronary disease, it was observed in one-third of individuals
hypertension [119]. Indexed LVM/bovine serum albumin (BSA) enables for
The American Society of Endocrinology defines normal LVM/BSA levels as
2
g/m
for women and 49–115 g/m
2
for men [118].
The 2021 ESC guidelines [91] and the 2022 AHA/ACC/HFSA updated guidelines
recommend natriuretic peptide biomarker screening (either NT-proBNP or
[120]
BNP)
to
identify diabetic patients with pre-HF. The 2022 AHA/ACC/HFSA guidelines
also
recommend routine assessment of circulating biomarkers in general for
supporting
with
by
the universal definition [90], routine screening of NT-proBNP or BNP is
recommended
levels
ing:
35
for hospitalized/decompensated HF patients, respectively [90]. Nevertheless,
mL
natriuretic
factors
increasing
mative
pendent
Frizzled-related
(TMAO),
a
diagnosis or exclusion of HF, risk stratification, and prognosis of patients
diabetes [120]. Since HF stages are defined by increased natriuretic peptide levels
in
patients without current or prior HF symptoms or signs. The cut-off
for BNP and NT-proBNP as settled by the universal definition were as follow-
pg/mL and 125 pg/mL for ambulatory HF patients and 100 pg/mL and 300 pg/
peptide levels are not sufficient to diagnose HF since CV and non-CV
diminish explanatory values of those levels under conditions such as AF,
age, obesity, and kidney disease [91]. In order to contribute to the infor-
diagnostic utility of natriuretic peptides, other new biomarkers, such as inde-
biomarkers for myocardial fibrosis or risk stratification in HF (secreted
proteins) or gut microbiota-derived trimethylamine N-oxide
are required [121–124].
6.4
Assessment of glycemic parameters in HF patients
When dysglycemia in patients with HFrEF remains undiagnosed, it is hard
to
determine a solid prognosis [125]. As a solution, the 2019 ESC-EASD
guidelines
previously
do
not yield a concrete result, it is recommended to perform OGTT [114]. The
2021
levels
comorbidities
6.5
advise testing HbA1c and FPG levels for detecting diabetes in patients
diagnosed with CVD [114]. Furthermore, if the aforementioned tests
ESC guidelines recommend to consistently check fasting glucose and HbA1c
if
chronic HF is suspected, to find its treatable causes and related
[91].
Strategies in people with diabetes to reduce the risk of HF
The 2019 ESC-EASD guidelines recommend regular microalbuminuria and eGFR
screening
other
guidelines
11
to
identify patients at high risk of renal dysfunction or future CVD. On the
hand, the Standards of Care 2021 from the ADA [126], and the 2019 ESC-EASD
[114] recommend a BP target of < 130/80 mmHg (but not < 120 mmHg).
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Moreover, even though the 2021 ESC guidelines [91] do not recommend a target, the
2022 AHA/ACC/HFSA guidelines [120] do recommend a more stringent target of
systolic BP of < 120 mmHg in individuals with diabetes at CV risk since hypertension
control is associated with a lower HF risk. It is worth noting that masked hypertension
(meaning only home, but not office BP levels are hypertensive) [127] is common in
T2D patients [128], making out-of-office BP monitoring a viable screening method for
this clinical condition [129, 130]. Diabetic and hypertensive patients should have their
ECGs checked at rest to identify silent MI, which happens in 4% of diabetic patients
and adds an insult to HF [114]. Additionally, for pre-diabetics and hypertensive
patients with diabetes, lifestyle adjustments and the use of RAAS blockers as first-line
therapy for BP management are advised [114]. RAAS blockers also diminish the
incidence of new-onset diabetes and the risk of sudden cardiac death in HFrEF
patients [114]. Aside from hypertension, a higher body mass index is thought to be a
risk factor for HF, which is why the ESC recommendations for 2021 [91] propose that
obesity should be controlled to avoid or delay the onset of HF.
7. Therapeutic considerations of HF in diabetes
Pharmacotherapy is the cornerstone of HFrEF treatment and should be used in con-
junction with non-pharmacological therapies before device therapy is considered [130].
Treatment for patients with HFrEF has three key goals: reduction in mortality,
avoiding recurrent hospitalizations due to worsening HF, and improving clinical status, functional capacity, and quality of life [130].
Patients with and without diabetes receive similar treatment for HF. On the other
hand, anti-diabetic drugs have different effects in patients with HF, and treatments
that are both safe and minimize HF-related events should be prioritized [130].
The 2021 ESC guidelines [91] and 2022 ACC/AHA/HFSA guidelines [120] recommend treatment of HFrEF and HFmrEF with a combination therapy of angiotensinconverting-enzyme inhibitors/angiotensin II receptor blockers (ACE-I/ARB),
angiotensin-receptor-neprilysin-inhibitors (ARNI), beta-blockers, mineralocorticoidreceptor antagonists (MRA), and SGLT2i. Since there is currently no therapy for
HFpEF subjects [91, 131], HFpEF therapy targets only symptom and well-being
improvement [91, 94] and treatment of comorbidities [91]. The recently reported
EMPEROR-preserved study provides the first proof of improved outcomes in HFpEF
individuals [132].
The 2021 ESC guidelines [91] also recommend that patients with improved LVEF
should continue to receive HFrEF treatment [91]. On the other hand, the 2021 ESC
guidelines recommend to use ICDs in selected patients with HFrEF of an ischemic
etiology and to consider using in those with a non-ischemic etiology [91]. Moreover,
CRT-P/D is recommended in those patients with HFrEF, in sinus rhythm, with an
LBBB ≥150 ms and should be considered in those with an LBBB ≥130–149 ms or nonLBBB ≥150 ms [91]. Advanced HF strategies, such as heart transplantation or MCS
may be appropriate in selected patients [91].
ACE-I and ARB: The effect of the ACE-I enalapril was demonstrated in the SOLVD
trial. It was shown that compared to placebo, enalapril diminished the incidence of
diabetes in subjects with HF [133]. The 2019 ESC-EASD recommendations suggest
blood pressure control with ACE-I or an ARB as a measure to lessen the HF risk in
diabetes, especially in conditions such as microalbuminuria, albuminuria, proteinuria,
or LV hypertrophy [99].
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The expediency of using ACE inhibitors in patients with insulin resistance is
by
explained
and
hyperglycemia, as well as by common molecular signal transduction pathways
by
used
ACE inhibitors or ARBs, continuous monitoring of potassium levels and renal
with
function
the activation of the RAAS against the background of hyperinsulinemia
the insulin and renin-angiotensin systems. When treating diabetic patients
is
necessary to prevent the development of nephropathy [134].
ARNI: In the PARADIGM-HF trial, it was observed that in comparison with enal-
sacubitril/valsartan is able to substantially reduce the death and hospitalization
april,
of HF
risk
effect
sacubitril/valsartan
compared
Moreover,
comparable
5.4–8.4%
HbA1c
both
enhance
(HHF) in people with HFrEF, demonstrating its blood pressure lowering
in
the long term [135]. However, in people with HFpEF, this trial showed that
was not effective at reducing the total CV death and HHF rate
to
valsartan alone (regardless of diabetes history in HFpEF patients) [136].
the positive impact of sacubitril-valsartan in reducing the risk of HHF was
among all PARADIGM-HF trial patients with HFrEF and an HbA1c of
[19]. Furthermore, sacubitril-valsartan outperforms enalapril in decreasing
levels and lowering the rate of insulin treatment initiation in individuals with
diabetes and HFrEF over 3 years [137]. Sacubitril-valsartan is thus expected to
glycemic control in these individuals [137].
A significant reduction in NT-proBNP levels was observed in the HFpEF group of
the
PARADIGM-HF trial [138], demonstrating that sacubitril-valsartan therapy
reduces
reduced
HFpEF
risk. This effect occurred regardless of gender, as sacubitril-valsartan equally
NT-proBNP levels in men and women in the PARAGON-HF cohort with
where 50% of subjects were diabetics [139].
There were a few observed side effects of sacubitril-valsartan therapy in the
PARADIGM-HF
Outcomes
increased
lower
[135].
that
prevalence of symptomatic hypertension and angioedema, but this was still
than with dual inhibition of both ACE and neprilysin, especially in angioedema
In
light of these data, the 2019 ESC-EASD Guidelines on diabetes recommend
HF
patients with diabetes who remain symptomatic should be treated with
sacubitril-valsartan
[135] and the Prospective Comparison of ARNI with ARB Global
in HF
with Preserved Ejection Fraction (PARAGON-HF trial) [136] such as
instead of an ACE inhibitor [114].
Beta-blockers: Beta-blockers have been shown to reduce mortality and morbidity
in
patients with HFrEF, when used together with ACE-I and diuretics [91]. As soon as
symptomatic
according
before
euvolemic patients at low doses and slowly uptitrated to the maximum tolerated
stable
dose.
Moreover, when patients are admitted with AHF in the hospital, beta-blockers
should
HFrEF is diagnosed, ACE-I and beta-blockers can be started together,
to
consensus. However, no evidence proves that starting a beta-blocker
an
ACE-I or vice versa is beneficial. Beta-blockers should be given to clinically
be
given cautiously only after they are hemodynamically stabilized [91].
There is no particular beta-blockade experiment in HFmrEF. The SENIORS trial, in
which
nebivolol lowered the composite main endpoint of all-cause mortality or CV
hospital
There
and
also
blocker
admissions in the total population, was included in an IPD meta-analysis.
was no interaction between LVEF (35–50% of patients had an LVEF of 35–50%)
the impact of nebivolol on the main outcome. Many patients with HFmrEF may
have another CV reason for a beta-blocker, such as AF or angina. As a result, beta-
therapy may be explored in individuals with HFmrEF [91].
MRA: Assessment of MRA therapy efficacy revealed that compared to non-MRA
treatment,
exact,
mortality
it
improved the clinical outcome of diabetic patients with HF [140]. To be
spironolactone or eplerenone was effective at diminishing CV and all-cause
and HHF [140]. A non-steroidal MRA finerenone, on the other hand, was
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able to reduce the incidence of death from any cause, CV-related hospitalization or
emergency in subjects with HFrEF, CKD, and/or diabetes when compared to
eplerenone MinerAlocorticoid Receptor antagonist Tolerability Study-Heart Failure
(ARTS-HF trial) [141].
Adverse events in the ARTS-HF and other MRA trials included in the aforementioned meta-analysis revealed that MRA treatment increases the risk of hyperkalemia
[140, 141].
Also, it has been shown that finerenone at doses of 10–20 mg/day may cause
hyperkalemia less frequently [142]. The drugs of this group can cause hyperkalemia
and deterioration of renal function, especially in the elderly, patients with diabetic
and non-diabetic nephropathy, renal failure; therefore, it is recommended to use them
only in patients with adequate renal function, while regular monitoring of plasma
electrolytes and renal function is mandatory.
Generally, the 2019 ESC-EASD recommendations [114] indicate that diabetic people with HFrEF should be treated with MRAs if their symptoms persist despite therapy with ACE-I or beta-blockers. In these patients, MRAs and sacubitril-valsartan are
indicated to minimize the risk of sudden cardiac death [114].
There is no MRA-specific study in HFmrEF. In a retrospective analysis of the
TOPCAT trial, spironolactone reduced hospitalizations for HF in patients with an
LVEF of ≥45%, but it increased hospitalizations for HF in those with an LVEF of
≥55%. A comparable trend was observed in CV mortality but not in all-cause mortality
[91]. Treatment with an MRA may be considered in patients with HFmrEF [91].
SGLT2 inhibitors: Numerous clinical trials have demonstrated the therapeutic
impact of SGLT2 inhibitors on CV outcomes in people with T2D and established HF,
demonstrating a cardio-protective effect independent of glycemic status [143].
Inhibition of SGLT2 increases the concentration of circulating ketone bodies, and it
can become an alternative source of energy for the diabetic heart with insulin resistance. In addition, other potential mechanisms of action of the drug are possible, such
as weight loss of the body, BP, sodium levels, oxidative stress, and sympathetic
activation [144]. One evidence comes from the DAPA-HF trial demonstrating that
dapagliflozin lowered the risk of progressing HF (HHF) and CV-related death in
HFrEF people (NYHA class II–IV) independent of the glycemic status [145] and
gender [146]. In addition, The Empagliflozin Outcome Trial in Patients with Chronic
Heart Failure with Preserved Ejection Fraction (EMPEROR)-preserved trial provided
the first evidence of a cardio-protective effect of empagliflozin on the combined risk
of HHF and CV death in subjects with HFpEF, an effect that is independent of the
presence of diabetes [132]. In other studies, for empagliflozin, a lowered risk of CV
death and HHF was also shown in the EMPA-REG OUTCOME trial in people with
T2D and a history of CVD [59] and in the EMPEROR-Reduced trial in people with
HFrEF regardless of the presence of diabetes [147].
One piece of evidence comes from the Dapagliflozin and Prevention of Adverse
Outcomes in Heart Failure (DAPA-HF) study, which found that dapagliflozin reduced
the risk of progressive HF (HHF) and CV-related death in patients with HFrEF
(NYHA class II–IV) regardless of glycemic status [145] or gender [146]. Furthermore,
the EMPEROR-preserved study showed the first indication of empagliflozin’s
cardioprotective benefit on the combined risk of HHF and CV death in people with
HFpEF, a result that is independent of diabetes [132]. In additional trials,
empagliflozin was associated with a decreased risk of CV mortality and HHF in the
EMPA-REG OUTCOME trial in patients with T2D and a history of CVD [59] and in
the EMPEROR-Reduced trial in people with HFrEF regardless of diabetes.
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Reducing the risk of CVD in empagliflozin includes combined decrease in blood
pressure,
ness
system,
heart
eNOS
cial
protein
slow
an
to
empagliflozin-induced
contribute
at
an
blood
systolic
diastolic
reduction
drug
dysfunction
microvascular
hyperglycemia
body weight (including visceral obesity), albuminuria, glucose levels, stiff-
of
the arterial wall, activation of the sympathetic part of the autonomic nervous
oxidative stress, uric acid concentration, and improvement function of the
[148]. Empagliflozin is able to improve myocardial microvascular perfusion,
activity, and endothelium-dependent relaxation. Empagliflozin may be benefi-
by
inhibiting induced DM mitochondrial fission dependent on 5’AMP-activated
kinase (AMPK) way. On the one hand, the action induced by this drug can
down the aging of endothelial cells by suppressing oxidative stress, which leads
improvement in their viability and barrier function. On the other hand,
migration endothelium as a result of F-actin homeostasis can
to
angiogenesis [59, 149]. As DM progresses endothelial damage is detected
early stage. Through these mechanisms, empagliflozin improves myocardial
supply. Considerable evidence suggests the ability of empagliflozin to reduce
blood pressure by facilitating osmotic diuresis, influencing the microvascular
response by stimulation of eNOS phosphorylation, vascular remodeling,
of
inflammatory proteins, and decrease in collagen synthesis [150]. This
is
promising for the treatment of patients with diabetes and microvascular
of
the heart; this drug can be considered as a drug for protecting the
bed of the heart to maintain its functions and circulatory structures in
[151].
In the Evaluation of Ertugliflozin Efficacy and Safety Cardiovascular Outcomes
(VERTIS CV trial), ertugliflozin was non-inferior to placebo in terms of its
Trial
important
atherosclerotic
(HR
risk
this
subgroups
< 60
SOLOIST-WHF
people
either
sotagliflozin
recent
secondary outcome of CV mortality or HHF in participants with T2D and
CVD, but the trial findings did not fulfill the superiority requirements
=
0.88, 95% CI 0.75–1.03) [61, 149]. However, there was a 30% reduction in the
of
HHF alone, which was similar to the effects of the other SGLT2 inhibitors on
outcome [149, 152]. A pre-specified analysis in VERTIS CV revealed that the
of
patients with the largest decrease in HF-related events had an eGFR of
mL/min/1.73 m
with T2D may reduce CV fatalities, hospitalizations, and urgent visits for
HFpEF or HFrEF [153]. When started before or shortly after discharge,
avoided CV death, HHF, and urgent HF visits in patients with T2D and
worsening HF compared to placebo.
2
and albuminuria [62]. Furthermore, another evidence from the
trial shows that simultaneous inhibition of both SGLT1 and SGLT2 in
SGLT2 inhibitors are cardio-protective in patients with T2D and established CVD,
also
in
people who are at high risk of CV events. The CANVAS study demonstrated
that
canagliflozin lowered the risk of CV-related events in people with T2D and
CV
increased
TIMI
58
people
risk more effectively than placebo [60]. Furthermore, the DECLARE-
study found that use of dapagliflozin reduces HHF and CV-related death in
with T2D who had or are at risk of atherosclerotic CVD [57].
NT-proBNPs have a predictive value for CV events and death in clinical outcome
studies.
CANVAS
with
tendency
function
[155].
higher
nificantly
The decreased NT-proBNP concentration in the canagliflozin arm of the
trial can be ascribed in part to the reduction in CV-related events in patients
T2D and CV risk [154]. In addition, a sub-analysis of the CANDLE study found a
toward decreased NT-proBNP levels in the subgroup with lower LV diastolic
in
the canagliflozin treated arm compared to the glimepiride treated arm
Dapagliflozin, like canagliflozin, reduced NT-proBNP levels considerably
than placebo in the DAPA-HF group [145, 149]. Similarly, empagliflozin sig-
lowered NT-proBNP levels 7 days after randomization when delivered as
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add-on treatment to T2D patients hospitalized for acute decompensated HF compared
to the group treated conventionally with glucose-lowering drugs [149, 156]. However,
another dual SGLT1/2 inhibitor, licogliflozin, has been shown to reduce NT-proBNP
in individuals with both T2D and HF when compared to placebo 12 weeks following
randomization [149, 157].
Because of the class impact of SGLT2 inhibitors, the 2019 ESC-EASD guidelines on
diabetes propose the SGLT2 inhibitors empagliflozin, canagliflozin, and dapagliflozin
to reduce the risk of HHF in diabetic individuals [114]. Aside from that, the ESC
guidelines for 2021 recommend ertugliflozin and sotagliflozin for patients with T2D
who are at high risk of CV events to reduce HHF, major adverse CV events (MACE),
end-stage renal disease, and CV death, and sotagliflozin in patients with T2D and
HFrEF to reduce HHF and CV death [91]. In order to minimize HHF, MACE, and CV
death, the 2019 ADA/EASD consensus suggests SGLT2 inhibitors in addition to metformin in adults with diabetes and HF (particularly HFrEF) [158].
8. Conclusion
HF is still a significant factor in life expectancy, especially among diabetic patients.
HF can be viewed as both a cause and a complication of DM at the same time.
Evidence strongly suggest that there is negative predictive effect of DM in the course
of HF. Therapy for this category of patients should be characterized by a holistic
approach, including a thorough glycemic control, as well as an effective blockade of
neurohumoral changes. New pharmacological options, such as SGLT2 inhibitors, are
allowing for better control of this life-threatening T2D condition. Biomarkers like NTproBNP can help identify HF early and predict prognosis and therapeutic efficacy of
HF or/and diabetes treatment. As a result, NT-proBNP testing should be used early in
the monitoring of subjects with diabetes with a high CV risk.
Acronyms and abbreviations
AAEDTE Azerbaijan Association of Endocrinology, Diabetology and
ACC American College of Cardiology
ACCF The American College of Cardiology Foundation
ACE-I angiotensin-converting-enzyme inhibitors
ADA American Diabetes Association
AF atrial fibrillation
AHA American Heart Association
AHF acute heart failure
AMPK 5
ARB angiotensin II receptor blockers
ARNI angiotensin-receptor-neprilysin-inhibitors
ATP adenosine triphosphate
BNP brain natriuretic peptide
BP blood pressure
BSA bovine serum albumin
CKD chronic kidney disease
CMiPD cardiomyopathy in people with diabetes
16
Therapeutic Education
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AMP-activated protein kinase
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cardiac resynchronization therapy with pacemaker/defibrillatorCRT-P/D
cardiovascular diseaseCVD
diabetes mellitusDM
dipeptidyl peptidase 4 inhibitorsDPP4
European Association for the Study of DiabetesEASD
electrocardiographyECG
estimated glomerular filtration rateeGFR
endothelial nitric oxide synthaseeNOS
European Society of CardiologyESC
fatty acidFA
fasting glucoseFG
fasting plasma glucoseFPG
glucagon-like peptide 1 receptor agonistGLP-1
glycohemoglobinHbA1c
heart failureHF
heart failure with mildly reduced ejection fractionHFmrEF
heart failure with preserved ejection fractionHFpEF
heart failure with reduced ejection fractionHFrEF
Heart Failure Society of AmericaHFSA
hospitalization for HFHHF
hazard ratioHR
implantable cardioverter defibrillatorICD
International Diabetes FederationIDF
impaired glucose metabolismIGM
impaired glucose toleranceIGT
individual patient dataIPD
left bundle branch blockLBBB
left ventricular ejection fractionLVEF
left ventricle massLVM
major adverse cardiovascular eventsMACE
mechanical circulatory supportMCS
myocardial infarctionMI
mineralocorticoid-receptor antagonistsMRA
normal glucose metabolismNGM
N-terminal pro-b-type natriuretic peptideNT-proBNP
New York Heart AssociationNYHA
oral glucose tolerance testOGTT
prediabetesPD
renin-angiotensin-aldosterone systemRAAS
sodium-glucose cotransporter 1SGLT1
sodium-glucose cotransporter 2SGLT2
sodium glucose co-transporter 2 inhibitorsSGLT2i
type 2 diabetesT2D
trimethylamine N-oxideTMAO
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