Авторы

  • А.Ya. Beshimov
    Bukhara State Medical University

DOI:

https://doi.org/10.71337/inlibrary.uz.cajei.126606

Ключевые слова:

Type 2 diabetes mellitus cardiomyopathy hot climate diastolic dysfunction myocardial remodeling environmental stress

Аннотация

This reformulated title underscores the integrated pathophysiological mechanisms and evolving clinical patterns of diabetic cardiomyopathy (DCM) in individuals with type 2 diabetes mellitus (T2DM) inhabiting hot climatic environments. The review delves into heat-related metabolic stressors, cardiovascular maladaptations, and proposes patient-centered, climate-conscious therapeutic models tailored for sustained cardiometabolic resilience..


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MULTISYSTEMIC DYNAMICS AND CLINICAL COURSE OF

CARDIOMYOPATHIC REMODELING IN TYPE 2 DIABETIC

PATIENTS EXPOSED TO HIGH THERMAL BURDEN:

STRATEGIC PERSPECTIVES ON INDIVIDUALIZED

MANAGEMENT

А.Ya.Beshimov

Bukhara State Medical University

https://doi.org/10.5281/zenodo.15755983

ARTICLE INFO

ABSTRACT

Qabul qilindi: 20-Iyun 2025 yil
Ma’qullandi: 24-Iyun 2025 yil

Nashr qilindi: 27-Iyun 2025 yil

This reformulated title underscores the integrated
pathophysiological mechanisms and evolving clinical
patterns of diabetic cardiomyopathy (DCM) in
individuals with type 2 diabetes mellitus (T2DM)
inhabiting hot climatic environments. The review delves
into heat-related metabolic stressors, cardiovascular
maladaptations, and proposes patient-centered,
climate-conscious therapeutic models tailored for
sustained cardiometabolic resilience..

KEY WORDS

Type

2

diabetes

mellitus,

cardiomyopathy,

hot

climate,

diastolic dysfunction, myocardial
remodeling, environmental stress

T2DM is widely acknowledged as a multifactorial disease exerting substantial

cardiovascular impact, with diabetic cardiomyopathy (DCM) emerging as a distinct and
progressive myocardial condition. Independent of ischemic and hypertensive origins, DCM is
increasingly recognized for its insidious onset and structurally degenerative course. In
environmentally extreme regions such as Central Asia and the Middle East, climatic variables
may significantly alter the pathophysiology and clinical manifestation of cardiac disease in
diabetic individuals.

Heat stress imposes additional burdens through mechanisms such as volume depletion,

electrolyte shifts, heightened sympathetic activity, and impaired circadian metabolic
regulation. These factors collectively compromise cardiac homeostasis and hinder
conventional management approaches. Given the paucity of focused regional data, this
investigation aims to define the pathoclinical features of DCM progression under chronic heat
exposure, facilitating informed intervention strategies.

Materials and Methods
An observational cohort of 120 patients (age 40–65) diagnosed with T2DM and early-

stage cardiomyopathic indicators was enrolled in Bukhara. Exclusion criteria included known
coronary artery disease, severe hypertension, and structural congenital anomalies. The study
spanned all seasonal phases across one year.

Assessed variables included:

Glycated hemoglobin (HbA1c), fasting plasma glucose, lipid indices

Biomarkers: NT-proBNP, hs-CRP

Echocardiography: LVEF, E/A ratio, LVMI, GLS

24-hour HRV and Holter monitoring

Environmental recordings: ambient temperature, humidity


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Patients were stratified into two groups based on ambient thermal exposure:

Group A: summer peak (≥38°C)

Group B: temperate months (<30°C)

Results
Participants in Group A exhibited statistically significant reductions in diastolic

performance (mean E/A: 0.84 ± 0.12 vs. 1.01 ± 0.10; p<0.01), elevated LVMI (128.6 ± 12.4
g/m²), and higher NT-proBNP levels. HRV analysis highlighted attenuated autonomic
responsiveness, particularly in SDNN and RMSSD indices. Nocturnal hypertension and
subclinical arrhythmias were markedly more prevalent during heat-exposure periods. Clinical
symptoms—fatigue, palpitations, and exertional breathlessness—intensified in Group A
during thermal surges. Multivariate modeling identified environmental heat, neurohormonal
stress markers, and HRV metrics as independent predictors of myocardial decline.

Table 1. Comparative Functional and Laboratory Data

Parameter

Group A (High Temp) Group B (Moderate Temp) p-value

E/A Ratio

0.84 ± 0.12

1.01 ± 0.10

<0.01

LV Mass Index

128.6 ± 12.4

114.3 ± 10.8

<0.05

NT-proBNP (pg/mL)

245 ± 38

180 ± 30

<0.01

SDNN (ms)

112 ± 15

135 ± 17

<0.05

Discussion
This study elucidates the potentiating effects of elevated environmental temperature on

cardiometabolic compromise in diabetic populations. The synergism between heat-induced
hemodynamic stress, neurohumoral dysregulation, and structural myocardial remodeling
contributes to accelerated disease progression. These findings support implementation of
seasonally-adjusted care pathways, incorporating tailored pharmacologic regimens, hydration
vigilance, and proactive cardiovascular monitoring.

Conclusion
Diabetic cardiomyopathy exhibits distinctive patterns of clinical deterioration in high-

temperature settings. Climatic context should therefore be a critical consideration in
cardiovascular risk assessment and management in T2DM care. Regional health systems must
evolve toward climate-integrated models of chronic disease oversight, prioritizing early
detection and intervention.

References:

1.

Maisch B, Alter P, Pankuweit S. Diabetic cardiomyopathy—fact or fiction? Herz.

2011;36(2):102–115.
2.

Rubler S, Dlugash J, Yuceoglu YZ, Kumral T, Branwood AW, Grishman A. New type of

cardiomyopathy associated with diabetic glomerulosclerosis. Am J Cardiol. 1972;30(6):595–
602.
3.

Boudina S, Abel ED. Diabetic cardiomyopathy revisited. Circulation. 2007;115(25):3213–

3223.
4.

Movahed MR, Hashemzadeh M, Jamal MM. Diabetes mellitus is a strong independent

predictor of diastolic dysfunction. Int J Cardiol. 2007;122(1):137–138.
5.

Lorenzo-Almorós A, Pello AM, Marín-Royo G, et al. Diagnostic approaches for diabetic


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cardiomyopathy. Cardiovasc Diabetol. 2017;16:28.
6.

Kovacic JC, Moreno P, Nabel EG, Hachinski V, Fuster V. Cellular senescence, vascular

disease, and aging. Part 1 of a 2-Part Review. Circulation. 2011;123(15):1650–1660.
7.

Jayasinghe S, Jayawardena R, Hills AP. Physical activity in South Asia: A narrative review.

Indian J Endocrinol Metab. 2016;20(5):588–595.
8.

Andersen CA, Andersson C, Berger JS, et al. Association between temperature and risk of

myocardial infarction in the United States. JAMA Cardiol. 2020;5(1):1–9.

Библиографические ссылки

Maisch B, Alter P, Pankuweit S. Diabetic cardiomyopathy—fact or fiction? Herz. 2011;36(2):102–115.

Rubler S, Dlugash J, Yuceoglu YZ, Kumral T, Branwood AW, Grishman A. New type of cardiomyopathy associated with diabetic glomerulosclerosis. Am J Cardiol. 1972;30(6):595–602.

Boudina S, Abel ED. Diabetic cardiomyopathy revisited. Circulation. 2007;115(25):3213–3223.

Movahed MR, Hashemzadeh M, Jamal MM. Diabetes mellitus is a strong independent predictor of diastolic dysfunction. Int J Cardiol. 2007;122(1):137–138.

Lorenzo-Almorós A, Pello AM, Marín-Royo G, et al. Diagnostic approaches for diabetic cardiomyopathy. Cardiovasc Diabetol. 2017;16:28.

Kovacic JC, Moreno P, Nabel EG, Hachinski V, Fuster V. Cellular senescence, vascular disease, and aging. Part 1 of a 2-Part Review. Circulation. 2011;123(15):1650–1660.

Jayasinghe S, Jayawardena R, Hills AP. Physical activity in South Asia: A narrative review. Indian J Endocrinol Metab. 2016;20(5):588–595.

Andersen CA, Andersson C, Berger JS, et al. Association between temperature and risk of myocardial infarction in the United States. JAMA Cardiol. 2020;5(1):1–9.