Chronic Obstructive Pulmonary Disease (COPD) remains a major cause of morbidity and mortality worldwide, particularly in low- and middle-income countries where exposure to smoking, biomass fuel, and environmental pollutants is widespread [1]. COPD is characterized by persistent airflow limitation that is not fully reversible and represents a major global cause of chronic morbidity and mortality [2]. COPD includes emphysema with alveolar destruction and enlargement, chronic bronchitis with chronic cough and phlegm, and small airway disease marked by narrowed bronchioles [3].

In many resource-limited settings, patients present late in the disease course, often with recurrent exacerbations and underdiagnosed comorbidities. Disease progression is often accelerated by recurrent exacerbations, which are associated with rapid declines in lung function and quality of life [4,5], and from which some patients never fully recover [6]. Cardiovascular disease is a common comorbidity and leading cause of death in COPD [7], reflecting the complex and interconnected pathobiological and clinical relationships between these conditions [8].

The common cardiovascular manifestations of chronic obstructive pulmonary disease include right ventricular dysfunction, pulmonary hypertension, coronary artery disease, and cardiac arrhythmias [9,10]. Although right ventricular dysfunction and pulmonary hypertension are common, increases in mean pulmonary artery pressure are usually mild to moderate [10]. The prevalence of pulmonary hypertension in COPD has been estimated at 20–30% and tends to worsen with increasing severity of airflow obstruction [11,12]. In a large cohort of nearly 400,000 patients, coronary artery disease was significantly more prevalent in individuals with COPD than in matched individuals without COPD. [13]. COPD is also associated with an increased risk of cardiac dysrhythmias, likely related to hypoxemia, acidosis, and reduced FEV₁ [14].

This study aims to characterize the clinical profiles, radiological features, and cardiological manifestations in patients with chronic obstructive pulmonary disease patients admitted with acute exacerbations in a tertiary care hospital.

Materials and Methods

This hospital-based observational study was conducted in the Department of Tuberculosis and Respiratory Diseases at a tertiary care hospital of North Kashmir region of India. Patients diagnosed with COPD according to standard clinical and spirometric criteria were enrolled over the study period. Patients with alternative causes of respiratory symptoms, significant structural heart disease unrelated to COPD, or incomplete clinical data were excluded.

All enrolled patients were informed about nature of the study and their rights to refuse. The informed written consent was taken from patients before including in the study. A structured proforma was used to record demographic details (age, sex, residence), smoking history (active, passive, ex-smoker, or non-smoker), duration of COPD, and prior hospitalization due to acute exacerbations. Clinical symptoms at presentation—including breathlessness, cough, fever, sputum production, oedema, and other associated complaints—were documented.

Radiological evaluation was done thorough chest X-rays. Cardiological assessment was done through echocardiography and echocardiography by a trained cardiologist. Echocardiographic assessments were performed to evaluate cardiac structure, systolic and diastolic function, valvular abnormalities, and pulmonary artery pressures. Left ventricular ejection fraction was recorded.

Data were compiled and analysed in Microsoft office excel. Continuous variables were expressed as mean ± standard deviation (SD), while categorical variables were presented as frequencies and percentages.

Results

The study population was predominantly elderly, with 70.4% of patients aged above 60 years. Females constituted a higher proportion (58.6%) than males (41.4%). Most patients were from rural areas (78.6%). Smoking exposure was present in 71.7% of participants, including active (20.0%), ex-smokers (29.7%), and passive smokers (22.1%). The majority had long-standing disease, with 64.9% having COPD for more than 10 years. Recent hospitalization in the past year was reported by 40.0% of patients. Most hospital stays were short, with 62.8% hospitalized for less than 7 days, while only 3.4% required hospitalization for 14 days or more. (Table 1)

Table 1. Sociodemographic and Clinical Characteristics of the Study Population

Breathlessness was the universal presenting symptom, reported by all patients (100%). Cough was present in 58.6% of cases, followed by fever (18.6%) and sputum production (16.6%). Systemic symptoms such as body ache or weakness were noted in 13.8% of patients. Features suggestive of fluid overload, including generalized body swelling (9.7%) and pedal oedema (4.8%), were less common. Nausea or vomiting was reported by 6.2% of patients, while other symptoms were observed in 11.7%. (Table 2)

Table 2. Distribution of Presenting Symptoms among the COPD patients

The most common chest X-ray finding was a tubular heart shadow (52.4%), followed by a low, flattened diaphragm (37.9%) and hypertranslucent lung fields (34.5%). Cardiomegaly was observed in 32.4% of patients. Consolidation was seen in 24.1%, and bilateral pleural effusion in 15.9%. Less frequent abnormalities included collapse (9.0%), unilateral pleural effusion (4.8%), and bilateral miliary mottling (3.4%). (Table 3)

Table 3. Chest X-ray Findings in COPD Patients

ECG abnormalities were frequently observed. First-degree atrioventricular block was the most common finding (16.6%), followed by negative P waves in limb leads (11.7%) and P pulmonale (9.7%). Axis deviations were also noted, with left axis deviation in 9.7% and right axis deviation in 8.3% of patients. Pathological Q waves were present in 8.3%. Atrial arrhythmias, including paroxysmal atrial fibrillation (6.2%) and atrial fibrillation (2.8%), along with other conduction abnormalities, were less frequently observed. (Table 4)

Table 4. Electrocardiographic Findings in Study Participants

Echocardiographic evaluation revealed mean ejection fraction of the study population around 56.5 ± 4.1%, with values ranging from 45% to 65%. The structural abnormalities were dominated by dilated RA/RV (40.7%) and dilated MPA (17.2%), while concentric LVH and RV hypertrophy were each present in 9% of patients. Diastolic dysfunction was common, with Grade 1 in 30.3% and Grade 2 in 15.9%. Valvular abnormalities were mainly tricuspid-related, with moderate TR being the most frequent finding (45.5%), followed by mild MR (24.8%) and moderate MR (16.6%). Pulmonary hypertension was also noted, predominantly moderate PAH (22.8%), with mild and severe PAH observed in 8.3% and 10.3% of cases, respectively. (Table 5)

Table 5. Echocardiographic Findings in the COPD Patients

DISCUSSION

Chronic obstructive pulmonary disease (COPD) is no longer regarded solely as a pulmonary disorder but a systemic endothelial disorder driven by age-related chronic inflammation affecting multiple organ systems. This persistent inflammatory state contributes to multimorbidity and explains the frequent coexistence of cardiovascular diseases in COPD patients [15,16]. Evidence indicates that low-grade inflammation persists during stable disease and intensifies during exacerbations, substantially increasing the risk of arrhythmias, ischemic heart disease, pulmonary hypertension, and heart failure [17,18]. Therefore, improved understanding of COPD–cardiovascular interactions is crucial, as early detection and prevention of cardiac comorbidities can significantly enhance clinical outcomes [19].

In this hospital-based observational study, we evaluated the clinical, radiological, and echocardiographic characteristics of patients presenting with acute exacerbations of COPD. Smoking exposure was identified in nearly three-fourths of patients, including active, ex-, and passive smokers, reaffirming smoking as a principal etiological factor for COPD [21,22]. However, the risk of COPD extends beyond conventional smoking patterns and includes a range of interrelated factors such as household and ambient air pollution, occupational exposures, early-life insults, recurrent infections, and socioeconomic disparities—particularly relevant in low- and middle-income countries [23].

Most patients had a disease duration exceeding 10 years, indicating long-standing COPD. Chronic hypoxia, persistent pulmonary vasoconstriction, and vascular remodeling in such patients predispose them to pulmonary hypertension and secondary cardiac involvement [10,24]. These findings emphasize the importance of longitudinal disease monitoring and integrated cardiopulmonary care.

Radiological abnormalities were common, with tubular heart shadow, hyperinflation changes, and cardiomegaly being the most frequent findings. These reflect chronic lung hyperinflation and secondary cardiac changes commonly observed in long-standing COPD. Consolidation and pleural effusion, although less frequent, may indicate infectious triggers or overlapping cardiac dysfunction.

Electrocardiographic abnormalities were frequently observed, reflecting both electrical conduction disturbances and structural cardiac changes. First-degree atrioventricular block was the most common ECG abnormality, possibly related to chronic hypoxia, electrolyte imbalance, or age-related degeneration of the conduction system. Atrial abnormalities such as negative P waves in limb leads and P pulmonale suggest right atrial enlargement secondary to chronic pulmonary disease [25]. Axis deviations further indicate ventricular remodeling and coexisting cardiac pathology.

Echocardiographic evaluation revealed a substantial burden of cardiac involvement. Right atrial and right ventricular dilatation were the most common structural abnormalities, consistent with findings from previous studies [26,27]. Chronic elevation of pulmonary arterial pressure in COPD leads to right ventricular dilation and hypertrophy, initially preserving stroke volume. However, during acute exacerbations, a sudden increase in right ventricular afterload may precipitate acute cor pulmonale and right heart failure [18,28]. However, the average ejection fraction remained within the normal range, indicating preserved left ventricular systolic function in the majority of patients.

Pulmonary vascular remodelling in COPD increases right ventricular afterload, and even clinically stable patients across all disease severities may harbor subclinical right ventricular dysfunction, highlighting the early and often unrecognized onset of cardiovascular comorbidities [29]. Dilatation of the main pulmonary artery and right ventricular hypertrophy further support the presence of long-standing pulmonary vascular disease [30]. Pulmonary hypertension was observed in 41.4% of patients, with moderate and severe pulmonary arterial hypertension noted in a significant proportion, consistent with prior reports [26,31]. Pulmonary hypertension in COPD is associated with increased exacerbation frequency and reduced survival, despite limited therapeutic options [32].

Additionally, lung hyperinflation and increased pulmonary vascular resistance due to hypoxic vasoconstriction contribute to elevated pulmonary artery pressures, which may impair right ventricular filling and lead to right ventricular diastolic dysfunction [33]. Left ventricular diastolic dysfunction was observed in nearly half of the patients, predominantly Grade 1 and Grade 2, corroborating findings from earlier studies [26,31]. Importantly, left ventricular diastolic dysfunction may occur even in the absence of systolic dysfunction or overt symptoms, yet is associated with heart failure and poorer prognosis [34,35]. Early detection of such dysfunction is therefore critical in the comprehensive management of patients with COPD.

CONCLUSION

COPD patients presenting with acute exacerbations exhibit significant pulmonary and cardiac manifestations. Chest X‑ray findings reflect chronic lung changes, while echocardiography demonstrates a high prevalence of pulmonary hypertension and right heart involvement. Routine radiological and echocardiographic evaluation should be considered essential in comprehensive COPD care. Further research with larger sample sizes and longitudinal follow-up is recommended to better understand long-term disease progression and the impact of cardiovascular disease in COPD.

REFERENCES

1. World Health Organization. Chronic obstructive pulmonary disease (COPD) [Internet]. Geneva: World Health Organization; 2024 [cited 2025 Dec 13]. Available from: https://www.who.int/news-room/fact-sheets/detail/chronic-obstructive-pulmonary-disease-(copd)
2. Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: A systematic analysis for the Global Burden of Disease Study. Lancet. 2012;380(9859):2095–2128.
3. Reilly, Silverman. chronic obstructive pulmonary disease. In: Kasper Dennis,Hauser Stephen, Jameson J. Larry, S. Fauci anthony, Longo, Loscalzo. Harrison's principles of internal medicine 19th edition, from New York, NY:McGraw Hill. 2015;2:1700.
4. Donaldson GC, Seemungal TA, Bhowmik A, Wedzicha JA. Relationship between exacerbation frequency and lung function decline in chronic obstructive pulmonary disease. Thorax. 2002;57:847–852.
5. Seemungal TA, Donaldson GC, Paul EA, Bestall JC, Jeffries DJ, Wedzicha JA. Effect of exacerbation on quality of life in patients with chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine. 1998;157:1418–1422.
6. Seemungal TA, Donaldson GC, Bhowmik A, Jeffries DJ, Wedzicha JA. Time course and recovery of exacerbations in patients with chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine. 2000;161:1608–1613.
7. Berry CE, Wise RA. Mortality in COPD: Causes, risk factors, and prevention. COPD. 2010;7:375–382.
8. Maeda T, Dransfield MT. Chronic obstructive pulmonary disease and cardiovascular disease: mechanistic links and implications for practice. Curr Opin Pulm Med. 2024 Mar 1;30(2):141-149.
9. Hunninghake D. Cardiovascular disease in chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2005;2:44–49.
10. Falk JA, Kadiev S, Criner GJ, Scharf SM, Minai OA, Diaz P. Cardiac disease in chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2008;5(4):543–548.
11. Burrows B, Kettel LJ, Niden AH, Rabinowitz M, Diener CF. Patterns of cardiovascular dysfunction in chronic obstructive lung disease. N Engl J Med. 1972;286:912–918.
12. Weitzenblum E, Sautegeau A, Ehrhart M, Mammosser M, Hirth C, Roegel E. Long-term course of pulmonary arterial pressure in chronic obstructive pulmonary disease. Am Rev Respir Dis. 1984;130:993–998.
13. Mapel DW, Dedrick D, Davis K. Trends and cardiovascular co-morbidities of COPD patients in the Veterans Administration medical system, 1991–1999. COPD. 2005;2:35–41.
14. Buch P, Friberg J, Scharling H, Lange P, Prescott E. Reduced lung function and the risk of atrial fibrillation in the Copenhagen City Heart Study. Eur Respir J. 2003;21:1012–1016.
15. Marcuccio G, Candia C, Maniscalco M, Ambrosino P. Endothelial dysfunction in chronic obstructive pulmonary disease: an update on mechanisms, assessment tools and treatment strategies. Front Med (Lausanne). 2025 Feb 12;12:1550716..
16. Rabe KF, Watz H. Chronic obstructive pulmonary disease. Lancet. 2017;389:1931–1940.
17. Schmidt SAJ, Johansen MB, Olsen M, Xu X, Parker JM, Molfino NA, et al. The impact of exacerbation frequency on mortality following acute exacerbations of COPD. BMJ Open. 2014;4:e006720.
18. André S, Conde B, Fragoso E, Boléo-Tomé JP, Areias V, Cardoso J. COPD and cardiovascular disease. Pulmonology. 2019;25(3):168–176.
19. Fabbri LM, Beghe B, Agusti A. Cardiovascular mechanisms of death in severe COPD exacerbation. Thorax. 2011;66:745–747.
20. Morgan AD, Zakeri R, Quint JK. Defining the relationship between COPD and CVD. Ther Adv Respir Dis. 2018;12:1753465817750524.
21. Laniado-Laborín R. Smoking and COPD. Int J Environ Res Public Health. 2009;6:209–224.
22. Buist AS, Vollmer WM, McBurnie MA. Worldwide burden of COPD. Int J Tuberc Lung Dis. 2008;12:703–708.
23. Cioboata R, Balteanu MA, Mitroi DM, Vrabie SC, Vlasceanu SG, Andrei GM, et al. Beyond smoking: emerging drivers of COPD. J Clin Med. 2025;14(13):4633.
24. Falk JA, Kadiev S, Criner GJ, Scharf SM, Minai OA, Diaz P. Cardiac disease in COPD. Proc Am Thorac Soc. 2008;5:543–548.
25. Roversi S, Fabbri LM, Sin DD, Hawkins NM, Agustí A.. COPD and cardiac diseases. Am J Respir Crit Care Med. 2016;194:1319–1336.
26. Harrigan RA, Jones K. Conditions affecting the right side of the heart. BMJ. 2002;324:1201–1204.
27. Islam KMN, Noor N, Begum AA, Hoque MJ, Rishad MM, Hossain A. Clinical profile and echocardiographic evaluation of COPD patients admitted in a tertiary care hospital. J Med. 2024;25(2):115–120.
28. Gosai JB, Parmar RK, Malaviya NM. ECG and echocardiographic findings in COPD exacerbations. J Chem Health Risks. 2024;14(4):1569–1573.
29. Pelà G, Li Calzi M, Pinelli S, Andreoli R, Sverzellati N, Bertorelli G, et al. Left ventricular remodeling in COPD. Int J Chron Obstruct Pulmon Dis. 2016;11:1015–1022.
30. Nasir SA, Singh S, Fotedar M, Chaudhari SK, Sethi KK. Right ventricular function in COPD. J Cardiovasc Echogr. 2020;30:125–130.
31. Raymond TE, Khabbaza JE, Yadav R, Tonelli AR. Main pulmonary artery dilation. Ann Am Thorac Soc. 2014;11:1623–1632.
32. Gupta NK, Agrawal RK, Srivastav AB, Ved ML. Echocardiographic evaluation of heart in chronic obstructive pulmonary disease patient and its co-relation with the severity of disease. Lung India. 2011 Apr;28(2):105-9.
33. Peinado VI, Pizarro S, Barberà JA. Pulmonary vascular involvement in COPD. Chest. 2008;134:808–814.
34. Rabe KF, Hurst JR, Suissa S. Cardiovascular disease and COPD. Eur Respir Rev. 2018;27:180057.
35. Cherneva Z, Valev D, Youroukova V, Cherneva R. Left ventricular diastolic dysfunction in COPD. PLoS One. 2021;16:e0247940.
36. Nagueh SF, Appleton CP, Gillebert TC, Marino PN, Oh JK, Smiseth OA, Waggoner AD, Flachskampf FA, Pellikka PA, Evangelisa A. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. Eur J Echocardiogr. 2009 Mar;10(2):165-93.