Woman in her seventh decade with huge heart in thorax

Abstract

This article reports a case of a 70-year-old female patient with severe tricuspid regurgitation (TR), aiming to supplement clinical data on isolated severe tricuspid insufficiency in elderly patients and provide references for etiological exploration and clinical decision-making (Writing Committee Members in J Am Coll Cardiol 77(4):e25–197, 2021). The patient had an 18-year history of recurrent bilateral lower extremity edema and a 3-year history of exertional fatigue and shortness of breath. Clinical examinations included echocardiography and enhanced chest computed tomography (CT). Echocardiography showed right atrial and ventricular enlargement, severe tricuspid regurgitation, and normal left ventricular systolic function; enhanced chest CT indicated significant enlargement of the heart (predominantly right atrium and ventricle), calcification of the aorta and coronary arteries, and a mass in the lower lobe of the right lung. The final diagnosis was severe tricuspid regurgitation (secondary to right heart dilation and tricuspid annulus dilatation), sinus rhythm, grade III cardiac function, and a right lower lung mass (nature to be determined) (Coisne et al. in J Am Coll Cardiol 82(8):721–34, 2023). Due to poor lung function and elevated arterial carbon dioxide partial pressure, the patient could not tolerate surgical treatment and was discharged with medication and follow-up recommendations. This case highlights the complexity of etiological diagnosis in elderly patients with isolated severe tricuspid insufficiency and the importance of comprehensive clinical assessment for treatment strategy formulation.

Introduction

Tricuspid insufficiency (TI), also known as tricuspid regurgitation, refers to the abnormal backflow of blood from the right ventricle to the right atrium during ventricular systole due to incomplete closure of the tricuspid valve. Clinically, TI is mostly secondary, with the most common etiology being right heart dilation and tricuspid annulus dilatation caused by various factors [1, 2]. In contrast, organic tricuspid lesions (e.g., rheumatic heart disease, infective endocarditis, and congenital tricuspid malformation) are relatively rare, accounting for only about 5–10% of all tricuspid valve diseases [3].

The prevalence of TI increases with age. Epidemiological studies show that in the general population over 65 years old, the prevalence of mild-to-moderate TI is approximately 15–20%, while severe TI has a relatively low prevalence of about 1–3%. However, severe TI is associated with poor prognosis, as it can lead to progressive right heart failure, systemic congestion, and even death if not properly managed. Most cases of severe TI are secondary to left heart disease (e.g., mitral valve disease, left ventricular systolic dysfunction), and isolated severe TI (without obvious left heart disease or pulmonary hypertension) in elderly patients is extremely rare, with only scattered case reports in the existing literature.

This case involves a 70-year-old female patient with isolated severe tricuspid regurgitation, without significant left heart structural or functional abnormalities. The case is valuable for enriching the clinical data of isolated severe TI in elderly patients, exploring its unique etiological characteristics, and optimizing clinical diagnosis and treatment strategies [4].

Case presentation

Patient information

The patient, Zhou Chongzhen, a 70-year-old female, was admitted to the Cardiac Surgery Department of West China Hospital, Sichuan University on July 22, 2020, due to “recurrent bilateral lower extremity edema for 18 years and exertional fatigue and shortness of breath for 3 years”. The medical history was provided by the patient herself, with high reliability.

Medical history

Eighteen years ago, the patient developed recurrent bilateral lower extremity edema accompanied by abdominal distension without obvious incentives, without chest tightness, palpitations, syncope, chronic cough, hemoptysis, or paroxysmal nocturnal dyspnea. She sought medical attention at a local hospital, where chest CT revealed a right lung mass, and she was diagnosed with “lung cancer”. Preoperative examination incidentally found tricuspid regurgitation, but the patient refused surgical treatment for lung cancer and was discharged with oral medications (specific drugs unknown). After treatment, the symptoms of edema and abdominal distension gradually relieved.

Three years ago, the patient began to experience fatigue and shortness of breath after mild activity (e.g., walking 200 m on flat ground), accompanied by recurrent bilateral lower extremity edema. The symptoms were not relieved by rest and were aggravated by cold or overexertion. She received diuretic treatment at a local hospital, and the symptoms were slightly relieved. In order to further diagnose and treat, she visited the outpatient department of our hospital. Echocardiography showed right heart enlargement and severe tricuspid regurgitation, and she was admitted to the hospital with the diagnosis of “severe tricuspid regurgitation” (Fig. 1).

Fig. 1.

A–D Transthoracic echocardiography of the giant heart patient

The patient denied a history of hepatitis, tuberculosis, or other infectious diseases; had no history of allergies, trauma, surgery, or blood transfusion; and had an unknown history of preventive vaccination. She had no smoking or drinking history and had long-term lived in her native place without a history of traveling to pastoral areas or epidemic areas. Her mother died of esophageal cancer, and her father’s cause of death was unknown; her siblings were in good health, with no family history of genetic diseases (Fig. 2).

Fig. 2.

12-lead electrocardiogram (ECG) of the giant heart patient

Physical examination

Vital signs: Temperature (T) was not recorded; pulse (P) 51 beats/min; respiratory rate (R) 22 breaths/min; blood pressure (BP) 112/58 mmHg; heart rate (HR) 51 beats/min; height 154 cm; weight 50 kg; body mass index (BMI) 21.0 kg/m².

The patient was conscious, with a natural expression, no obvious illness appearance, normal development, good nutrition, autonomous posture, normal gait, and cooperative with physical examination. No rash or subcutaneous hemorrhage was found on the whole body; no enlarged superficial lymph nodes were palpable. No abnormalities were found in the head and neck. Bilateral lungs were dull on percussion; breath sounds were clear; no dry or wet rales were heard; bilateral respiratory movements were symmetrical, without enhancement or weakening; bilateral tactile fremitus was symmetrical and normal; no pleural friction rub was felt (Figs.  2, 3).

Fig. 3.

A Chest contrast-enhanced CT (coronal plane). B Chest contrast-enhanced CT 3D reconstruction. C Chest contrast-enhanced CT (sagittal plane)

Heart (tricuspid insufficiency-related signs): The heart boundary was normal (no obvious enlargement of the right heart was found by percussion, which may be related to the limited sensitivity of percussion examination; echocardiography showed obvious right atrial and ventricular enlargement). The heart rhythm was regular (sinus rhythm at the time of examination). The first heart sound at the tricuspid area was weakened; the second heart sound was normal; no third or fourth heart sound was heard. A grade 3/6 systolic blowing murmur was heard at the 4th–5th intercostal space on the left sternal border, which was enhanced during inspiration and weakened during expiration (Carvallo sign positive). The murmur radiated to the right lower sternal border and the xiphoid process, and its intensity was related to the degree of tricuspid regurgitation.

The abdomen was flat and soft, with no tenderness or rebound tenderness; no abdominal masses were palpable; the liver and spleen were not palpable under the costal margin; no edema was found in the extremities (edema was relieved after diuretic treatment before admission); no abnormalities were found in the joints; pathological signs were negative.

Auxiliary examinations

Echocardiography

The right atrium was significantly enlarged (giant right atrium); the right ventricle was enlarged; the left atrium and ventricle were of normal size. The tricuspid annulus was dilated, with an annulus diameter of about 60 mm; the valve leaflets were normally attached, with reduced mobility and obvious closure gaps; no obvious abnormalities were found in the morphology and structure of other valves (mitral valve, aortic valve, pulmonary valve). The main pulmonary artery and pulmonary artery branches were of normal diameter; the atrial and ventricular septa were continuous, without defects; the thickness and amplitude of the ventricular septum and left ventricular posterior wall were normal; the overall movement of the left ventricular wall was coordinated. A small amount of pericardial effusion was found; no obvious abnormalities were found in the proximal segment of the aortic arch and descending aorta. There was severe tricuspid regurgitation, with peak regurgitation velocity (Vmax) = 2.3 m/s and pressure gradient (PG) = 21 mmHg. The aortic valve had slight acceleration of forward blood flow (Vmax = 2.0 m/s) and a small amount of regurgitation under the valve. No abnormal blood flow signals were detected on both sides of the other valve orifices; no definite shunt was found in the heart. Left ventricular systolic function was normal (specific values were not provided in the report, but no abnormality was indicated) (Fig. 1).

Enhanced chest CT

The heart was extremely enlarged, mainly involving the right atrium and right ventricle; the muscular part of the atrioventricular septum was partially unclear (suggesting possible myocardial remodeling due to long-term right heart overload); the superior and inferior vena cava were significantly dilated (consistent with right heart insufficiency and increased central venous pressure); calcification was found in the aorta and left and right coronary arteries (suggesting arteriosclerosis).A small amount of pericardial effusion was present. A mass was found in the outer basal segment of the right lower lung, with calcification inside; the possibility of a benign lesion was high (excluding malignant tumors as the direct cause of tricuspid regurgitation); a small amount of scattered inflammatory foci were found in both lungs (Fig. 3).

Diagnosis and clinical course

Final diagnosis

1. Cardiac valve disease: Severe tricuspid regurgitation (secondary to right heart dilation and tricuspid annulus dilatation).

2. Cardiac rhythm: Sinus rhythm.

3. Cardiac function: Grade III (New York Heart Association, NYHA classification).

4. Right lower lung mass (nature to be determined, considering benign lesions).

Clinical course

After admission, the patient completed relevant examinations such as echocardiography and enhanced chest CT. The results showed severe tricuspid regurgitation, right heart enlargement, and respiratory insufficiency (elevated carbon dioxide partial pressure). The medical team evaluated the patient’s surgical tolerance and found that her poor lung function made her unable to tolerate tricuspid valve replacement or repair surgery.

During hospitalization, symptomatic treatment such as diuresis was given to relieve systemic congestion; respiratory function was monitored and improved; and the patient and her family were fully communicated about the condition and treatment options.

After 5 days of hospitalization, the patient’s general condition was stable, with no chest tightness, palpitations, or shortness of breath; vital signs were stable (HR 95 beats/min, rhythm regular); a systolic murmur was still heard at the 4th–5th intercostal space on the left sternal border; bilateral lung breath sounds were slightly rough, with no dry or wet rales; no lower extremity edema was found.

Discharge recommendations: First, maintain a balanced diet, avoid excessive salt intake, and improve nutritional status. Second, continue respiratory function treatment in the respiratory department; re-evaluate the possibility of tricuspid valve surgery in the outpatient department after lung function improvement. Third, take discharge medications as prescribed: Potassium chloride sustained-release tablets 500 mg orally, 3 times a day (to prevent hypokalemia caused by diuretics); spironolactone tablets 20 mg orally, once a day (potassium-sparing diuretic, reducing systemic congestion); furosemide tablets 20 mg orally, once a day (loop diuretic, relieving edema); tolvaptan tablets (Samsca) 15 mg orally, once a day (aquaretics, reducing water retention without affecting electrolyte balance). Fourth, seek medical attention immediately if symptoms such as aggravated shortness of breath, recurrent severe lower extremity edema, chest pain, or syncope occur.

Discussion

Etiological analysis of isolated severe tricuspid regurgitation in this case

Severe tricuspid regurgitation in elderly patients is mostly secondary to left heart disease (e.g., mitral stenosis, left ventricular systolic dysfunction leading to pulmonary hypertension and right heart overload) or pulmonary diseases (e.g., chronic obstructive pulmonary disease leading to pulmonary hypertension). However, this patient had normal left ventricular structure and function (echocardiography showed no left atrial and ventricular enlargement, and normal left ventricular wall movement), and no obvious pulmonary hypertension-related signs (pulmonary artery diameter was normal, and tricuspid regurgitation pressure gradient was 21 mmHg, suggesting mild pulmonary hypertension or normal pulmonary artery pressure). Therefore, it belongs to isolated severe tricuspid regurgitation, which is rare in clinical practice.

Combined with the patient’s medical history and examination results, the possible etiologies are analyzed as follows: First, secondary tricuspid regurgitation due to idiopathic right heart dilation. The patient had no obvious causes of right heart overload (such as pulmonary hypertension, congenital heart disease, or pulmonary embolism), but echocardiography and enhanced CT showed significant right atrial and ventricular enlargement and tricuspid annulus dilatation (60 mm, normal value < 40 mm). Long-term right heart dilation may lead to tricuspid valve leaflet malcoaptation and severe regurgitation, which is consistent with the “volume overload-induced tricuspid regurgitation” mechanism proposed in the literature. Second, the relationship between right lung mass and tricuspid regurgitation. The patient had a right lung mass (considering benign lesions), but there was no evidence that the mass invaded the heart or pulmonary vessels, so it was not the direct cause of tricuspid regurgitation. However, if the mass had caused long-term mild pulmonary ventilation dysfunction (even without obvious clinical symptoms), it might have led to chronic subclinical right heart overload, which could not be excluded as an indirect contributing factor. Third, age-related tricuspid valve degeneration. Elderly patients may have degenerative changes in the tricuspid valve (such as leaflet thickening and chordae tendineae relaxation), but echocardiography showed no obvious organic lesions of the tricuspid valve leaflets, so this possibility was ruled out.

Clinical value of comprehensive diagnostic modalities in tricuspid insufficiency

The diagnosis of tricuspid insufficiency requires a combination of multiple modalities to clarify the etiology and severity. Echocardiography is the first-line examination method, which can directly evaluate the structure (annulus diameter, leaflet morphology) and function (regurgitation degree, ventricular size) of the tricuspid valve. In this case, echocardiography clearly showed severe tricuspid regurgitation and right heart enlargement, providing the core diagnostic basis. Enhanced chest CT can evaluate the anatomical relationship between the heart and surrounding organs (such as the right lung mass) and the dilation of the great vessels (superior and inferior vena cava), helping to exclude extracardiac causes of tricuspid regurgitation.

Treatment dilemma and follow-up strategy

For severe tricuspid regurgitation, surgical treatment (tricuspid valve replacement or repair) is the only way to achieve radical cure, but it is limited by the patient’s surgical tolerance. This patient had poor lung function and elevated carbon dioxide partial pressure, so she could not tolerate surgery temporarily. The follow-up treatment strategy should focus on three aspects: First, medical treatment optimization. Long-term use of diuretics (furosemide, spironolactone) and aquaretics (tolvaptan) to control systemic congestion and improve quality of life; regular monitoring of electrolyte levels to prevent hypokalemia or hyperkalemia. Second, respiratory function improvement. Cooperation with the respiratory department to treat lung inflammation and improve lung function, creating conditions for subsequent surgical evaluation. Third, regular follow-up. Recheck echocardiography every 3–6 months to monitor the progression of right heart enlargement and tricuspid regurgitation; re-evaluate surgical feasibility once lung function is improved.

Limitations of this case and future research directions

The limitations of this case include missing data from some examinations (such as electrocardiography, chest X-ray, cardiac magnetic resonance imaging, cardiac catheterization) due to the patient’s situation, which affects the comprehensiveness of etiological analysis; and lack of long-term follow-up data to observe the progression of the disease and the effect of medical treatment. Future research on isolated severe tricuspid regurgitation in elderly patients should focus on expanding the sample size to explore its epidemiological characteristics and common etiologies; comparing the efficacy of different surgical methods (valve repair vs. replacement) in elderly patients; and exploring the value of minimally invasive interventional therapy (such as transcatheter tricuspid valve repair) for high-risk patients who cannot tolerate open surgery.

Author contributions

WC and CS was involved in drafting the manuscript. LH is responsible for the collection and organization of images from CT imaging, electrocardiograms (ECG), and other examinations.WC and CS was made contributions to the concepts, acquisition and analysis of the data. CS and LH was involved in acquisition of data and preparing the Tables. WC and CS designed and revised the manuscript. All authors have read and approved the final manuscript.

Funding

This paper was supported by the Natural Science Foundation of Sichuan Province (No. 2024NSFSC1924) (to Cheng SHEN).

Data availability

All data for this study are publicly available and are ready for the public from database of hospital.

Declarations

Ethics approval and consent to participate

Informed written consent and institutional review board approval were both obtained from West China Hospital Ethics Committee (No. 202235) and affiliation of ethics committee for the surgery and the publication of the study.

Consent for publication

All the authors consent to publish the paper.

Competing interests

The authors declare no competing interests.