In the present study, we evaluated left ventricular
systolic function using GLS in patients with CSF
and compared strain parameters between treated
and untreated individuals. Our study demonstrated
that patients with CSF exhibited subclinical left
ventricular systolic dysfunction, as evidenced by
reduced GLS, despite preserved LVEF. More
importantly, patients receiving pharmacological
treatment had significantly better GLS values,
suggesting that medical treatment may improve
myocardial deformation and potentially enhance
myocardial perfusion at the microvascular level.
Coronary slow flow is considered a microvascular
disorder involving endothelial dysfunction,
inflammation, and impaired vasomotor regulation.[2]
These mechanisms contribute to myocardial ischemia
and contractile impairment, which may not always
be apparent with conventional echocardiographic
parameters, but can be sensitively detected by
strain imaging.[4] Pharmacological agents such as
beta-blockers, calcium channel blockers, and statins
have previously been shown to improve endothelial
function and microvascular circulation,[5] consistent
with our observation of improved GLS values in the
treated group.
In the current study, although LVEF was preserved
in both groups, untreated CSF patients exhibited significantly impaired GLS compared to those
receiving pharmacological treatment, suggesting that
medical treatment improves subclinical myocardial
function. These findings are consistent with previous
reports emphasizing the incremental diagnostic value
of strain imaging for detecting subtle myocardial
dysfunction[4] and align with evidence demonstrating
the beneficial effects of pharmacological treatment on
coronary microvascular function and left ventricular
performance in CSF patients.[11,12] Collectively, our
results support the role of GLS as a sensitive marker
for monitoring therapeutic efficacy and underscore
the importance of medical treatment in improving
myocardial mechanics in CSF.
The diagnostic and prognostic value of GLS
has also been demonstrated in other cardiovascular
conditions. Şenöz et al.[13] reported that hemodialysis
patients with preserved LVEF exhibited impaired
GLS, underscoring the sensitivity of STE in
unmasking subtle myocardial dysfunction. Similarly,
Durak et al.[14] showed that the Fibrosis-4 index was
associated with left atrial volume index in patients
with acute coronary syndrome, emphasizing the
growing importance of deformation-based parameters
in cardiovascular risk stratification. These studies
support our findings by highlighting that strain
imaging provides incremental diagnostic information
beyond LVEF in diverse clinical populations.
Our results are also consistent with findings
from CSF-specific studies. Shawky Shereef et
al.[15] demonstrated that patients with CSF had
significantly lower GLS compared to controls, and
GLS was strongly correlated with the TIMI frame
count (−16.18±1.25 vs. −19.34±1.33; p<0.001). They
further identified impaired GLS as an independent
predictor of CSF when a cut-off of −17.8% was applied,
reinforcing the diagnostic role of strain imaging in
this population. Beyond cardiac dysfunction, Ito and
Mori[16] highlighted the relevance of GLS in the cardio-renal-brain axis, showing its association with
systemic dysfunction, including cognitive impairment.
Although not specific to CSF, this underscores the
broader systemic implications of impaired myocardial
strain and supports its role as an integrative biomarker
of microvascular disease.
Patients with CSF showed preserved LVEF,
but impaired GLS, indicating subclinical systolic
dysfunction. Treatment was associated with improved
GLS, suggesting a favorable effect on microvascular
function. Consistent with our findings, the recently
proposed MAPH score by Akhan and Kış[17] emphasizes
the contribution of hemorheological factors to CSF,
supporting the need for early recognition and targeted
management.
In our cohort, GLS values were significantly
improved in patients receiving pharmacological
treatment, suggesting that treatment may exert
protective effects at both the myocardial and
microvascular levels. While age and comorbidities
such as hypertension and smoking are known to
influence ventricular strain, the consistency of our
findings with prior studies suggests that the observed
improvement in GLS is likely treatment-related
rather than solely attributable to baseline patient
characteristics.
Taken together, our study and existing evidence
highlight the utility of GLS in detecting subtle
myocardial dysfunction in CSF and support the role
of medical treatment in minimizing its adverse effects.
Early detection of subclinical impairment using
strain echocardiography and timely pharmacological
intervention may, therefore, be crucial in improving
long-term outcomes in CSF patients.
The main limitation to this study is its
relatively small sample size, which may restrict the
generalizability of our findings. Further multi-center,
large-scale studies are needed to confirm these
results and better define the impact of treatment on
myocardial function in patients with CSF.
In conclusion, in patients with CSF, subclinical
left ventricular systolic dysfunction can be detected
using GLS, despite preserved LVEF. Pharmacological
treatment is associated with improved myocardial
strain parameters, suggesting a protective effect on
myocardial function. Early diagnosis and management
of CSF may improve long-term cardiac outcomes.
Further prospective studies with larger populations are warranted to confirm these findings and optimize
treatment strategies.
Data Sharing Statement: The data that support the
findings of this study are available from the corresponding
author upon reasonable request.
Conflict of Interest: The author declared no conflicts of
interest with respect to the authorship and/or publication of
this article.
Funding: The author received no financial support for the
research and/or authorship of this article.
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