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Year : 2021  |  Volume : 11  |  Issue : 4  |  Page : 198-200

Giant right ventricular clot: Smoking is injurious to veins!

1 Department of Cardiology, Yashoda Hospitals, Hyderabad, Telangana, India
2 Department of Internal Medicine, Yashoda Hospitals, Hyderabad, Telangana, India
3 Department of Critical Care Medicine, Yashoda Hospitals, Hyderabad, Telangana, India

Date of Submission10-Dec-2020
Date of Decision14-Dec-2020
Date of Acceptance18-Dec-2020
Date of Web Publication25-Oct-2021

Correspondence Address:
Dr. Pankaj Jariwala
Department of Cardiology, Yashoda Hospitals, Somajiguda, Raj Bhavan Road, Hyderabad - 500 082, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jicc.jicc_86_20

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Giant right ventricular thrombus is a rare characteristic of pulmonary thrombosis-embolism that is typically associated with chronic obstructive pulmonary disease (COPD) exacerbation. We found such a giant right ventricular thrombus in a patient who was a heavy smoker who had extreme type of COPD with cor pulmonale. He also had hypotension, hypoxia, low tolerance for exercise, congestive heart failure, and poor quality of life, which are the prognostic qualities in the patient's clinical scenario we mentioned.

Keywords: Chronic obstructive pulmonary diseases, deep venous thrombosis, pulmonary embolism, venous thromboembolism

How to cite this article:
Jariwala P, Jadhav KP, Boorugu H, Punjani A, Mishra KC. Giant right ventricular clot: Smoking is injurious to veins!. J Indian coll cardiol 2021;11:198-200

How to cite this URL:
Jariwala P, Jadhav KP, Boorugu H, Punjani A, Mishra KC. Giant right ventricular clot: Smoking is injurious to veins!. J Indian coll cardiol [serial online] 2021 [cited 2023 Feb 3];11:198-200. Available from: https://www.joicc.org/text.asp?2021/11/4/198/329157

  Introduction Top

Chronic obstructive pulmonary disease (COPD) patients are often admitted to hospital for an exacerbation of their condition that presents for worsening dyspnea, chest pain, and ankle edema. All COPD is a considered risk factor for pulmonary embolism (PE), but the symptoms of these conditions greatly differ and PE diagnosis in these cases is either overlooked or delayed. A coexisting COPD can be believed to be the cause of the symptoms of the patient, and the presence of PE will go undiagnosed in patients who can handle it the least.

  Case Report Top

A 48-year-old male, chronic smoker (5–6 packs/year) and known case of COPD, has been admitted with the complaints of progressive breathlessness for the last 15 days. Vital parameters recorded blood pressure of 80/60 mmHg, pulse rate of 112/min, respiratory rate of 30/min, and room air oxygen saturation of 78%. Basic cardiorespiratory support, with the aid of noninvasive ventilation, did not improve enough that hemodynamics and respiratory parameters could be improved by endotracheal intubation and inotropic treatment.

Echocardiography demonstrated global hypokinesia of the left ventricle (ejection fraction – 28%) with dilatation of the right ventricle (RV) and atrium. There was large clot attached to free wall, apical segments that occupied more than two-third of RV [Figure 1]a, [Figure 1]b, [Figure 1]c and Videos 1 and 2]. Mild tricuspid regurgitation recorded RV systolic pressure of 55 mmHg. There was no evidence of any venous thromboembolism (VTE). Laboratory parameters showed multiple hematological abnormalities such as neutrophilic leukocytosis, deranged coagulation parameters such as elevated prothrombin time and D-dimer levels, elevated hepatic enzymes, direct hyperbilirubinemia, elevated serum creatinine, blood urea, and brain natriuretic peptide levels. Computed tomography of the pulmonary vasculature could not be done to demonstrate pulmonary thromboembolism (PE) as the patient was hemodynamically unstable. The patient was supervised in intensive cardiac care unit, and inotropic treatment was provided in the form of intravenous noradrenaline, dobutamine through the central line catheter. Low-molecular-weight heparin, enoxaparin 1 mg/kg was given twice daily along with 150 mg of oral aspirin. Higher-generation antibiotics were also initiated in the form of a combination of cefoperazone and azithromycin while awaiting results of the blood and endotracheal cultures. Additional respiratory supportive and total parenteral nutrition was offered. On the 3rd day of admission, the patient became hemodynamically unstable requiring higher doses of the inotropes to maintain his blood pressure.
Figure 1: (a-c) Transthoracic echocardiography in modified four-chamber view with medial angulation of the probe revealed a giant right ventricular clot fixed to the right ventricle free wall which looked like “fetus in utero” appearance (a; white asterisk). Subcostal views demonstrated the extent of RV clot to the apex of the right ventricle (c, white arrow) and further anterior angulation could delineate the entire apico-anterior extension of it (c, white arrow). RV = Right ventricle, RA = Right atrium, LV = Left ventricle, IVS = Interventricular septum, TV = Tricuspid valve

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The patient had bleeding diathesis with deranged coagulation parameters such as elevated prothrombin time and thrombocytopenia, hence could not administered any thrombolytic therapy nor he was fit for any cardiothoracic surgical intervention. Renal parameters deteriorated further requiring renal replacement therapy. The patient could not be saved by conscientious management of multimodality and died secondary to multiorgan failure and bleeding diathesis.

  Discussion Top

Severe COPD patients may have a higher risk of secondary VTE, and COPD patients with VTE may have a higher mortality rate than COPD patients without VTE.[1] VTE in COPD was significantly correlated with body mass index, exercise tolerance, and other associated medical comorbidities. In patients with dyspnea, physicians should suspect VTE and should recognize causes other than infection as triggers of the worsening of COPD.[2] D-dimer levels and Wells criteria should be used to ascertain whether or not these patients are being evaluated for the risk of PE.[3]

The prevalence of PE was 29.1% in the analysis by Akpınar et al. Patients with pleuritic chest pain, lower limb asymmetry, and elevated NT-pro-BNP were much more likely to develop PE than those who were obese or immobile.[4] Bertoletti et al. analyzed COPD patients enrolled under the worldwide RIETE registry, including 4036 COPD patients; 61% had PE and a higher rate of VTE recurrence, severe bleeding complications, and fatal PE.[5] In the COPD Genetic Epidemiology report, the Global Initiative for Chronic Obstructive Lung Disease stage II–IV participants were divided into two groups with or without VTE. The positive VTE group had older, smoking history, oxygen usage, a walking distance of <6 min, poorer quality of life, and more respiratory aggravation than that of the VTE-negative group.[2]

The International Cooperative Pulmonary Embolism Registry examined the prognostic value of right heart thrombi(RHT) in PE. RHT patients had shorter symptom length, lower systolic blood pressure, and more severe right ventricular hypokinesis and congestive heart failure.[6],[7] In our scenario, all the negative attributes substantiate bad outcome as linked by most of them.

In our situation, we did not offer thrombolysis because the patient had bleeding diathesis, and in this subgroup of patients, there are no specific guidelines relating to the option of treatment. Randomized controlled trials investigating the efficacy of reperfusion therapies in this group of patients will provide better insight into which intervention would lead to improved outcomes.

  Conclusion Top

Patients with underlying COPD had increased tendency to develop VTE and fatal PE, but formation of giant RV clot is rare. In these circumstances, the presence of giant RV clot associated with hemodynamic instability, bleeding diathesis, deranged metabolic parameters, and multiorgan dysfunction are poor prognostic factors and carry a high mortality despite treatment.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Børvik T, Brækkan SK, Enga K, Schirmer H, Brodin EE, Melbye H, et al. COPD and risk of venous thromboembolism and mortality in a general population. Eur Respir J 2016;47:473-81.  Back to cited text no. 1
Kim V, Goel N, Gangar J, Zhao H, Ciccolella D, Silverman E, et al. Risk factors for venous thromboembolism in chronic obstructive pulmonary disease. Chronic Obstr Pulm Dis J COPD Found 2014;1:239-49.  Back to cited text no. 2
Gunen H, Gulbas G, In E, Yetkin O, Hacievliyagil SS. Venous thromboemboli and exacerbations of COPD. Eur Respir J 2010;35:1243-8.  Back to cited text no. 3
Akpınar EE, Hosgün D, Akpınar S, Ataç GK, Doganay B GM. Incidence of pulmonary embolism during COPD exacerbation. J Bras Pneumol 2014;13:173-82.  Back to cited text no. 4
Bertoletti L, Quenet S, Laporte S, Sahuquillo JC, Conget F, Pedrajas JM, et al. Pulmonary embolism and 3-month outcomes in 4036 patients with venous thromboembolism and chronic obstructive pulmonary disease: Data from the RIETE registry. Respir Res 2013;14:1-8.  Back to cited text no. 5
Torbicki A, Galié N, Covezzoli A, Rossi E, De Rosa M, Goldhaber SZ. Right heart thrombi in pulmonary embolism: Results from the International cooperative pulmonary embolism registry. J Am Coll Cardiol 2003;41:2245-51.  Back to cited text no. 6
Sabit R, Bolton CE, Fraser AG, Edwards JM, Edwards PH, Ionescu AA, et al. Sub-clinical left and right ventricular dysfunction in patients with COPD. Respir Med 2010;104:1171-8.  Back to cited text no. 7


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