How is pulmonary thromboembolism in combination with left heart disease diagnosed?

How to diagnose left heart disease combined with pulmonary thromboembolism?
Pulmonary Vascular Disease Center, Fu Wai Cardiovascular Hospital, Chinese Academy of Medical Sciences
Changming Xiong
Left heart diseases such as hypertension, coronary artery disease, cardiomyopathy and valvular disease with cardiac insufficiency can present with chest tightness and shortness of breath after activity, which are similar to the symptoms of pulmonary thromboembolism (pulmonary embolism). In this paper, we discuss the clinical characteristics of pulmonary embolism combined with left heart disease with the aim of improving the diagnosis of pulmonary embolism and reducing the underdiagnosis of pulmonary embolism combined with left heart disease by combining 2 case studies. Xiong Changming, Department of Cardiovascular Medicine, Fu Wai Hospital, Beijing, China
Case 1, a male, 67 years old, was admitted to the hospital with episodes of chest tightness for 8 years and a previous history of diabetes and hypertension. After admission, a coronary angiogram was performed, suggesting a lesion in three branches of the coronary artery. He then underwent coronary artery bypass grafting. 1 week after the operation, he started to have intermittent fever, with temperature fluctuating from 37.5℃ to 38.5℃. Physical examination: BP: 110/70 mmHg, left lower lung breath sounds were weak, no dry and wet rales were heard, HR 86 beats/min, rhythmical, no murmur was heard in each valve auscultation area, no edema in both lower limbs. Laboratory tests: Arterial blood gas analysis: pH 7.50, PO2 59.7mmHg, PCO2 29.8mmHg, HCO3- 23.2mmol/L. D-dimer 10.29μg/ml. Chest X-ray: heavy texture in both lungs, left ventricle is large, small amount of pleural effusion bilaterally. Electrocardiogram: sinus rhythm, ST-T changes. Echocardiogram: left atrium 35 mm, left ventricular end-diastolic meridian 53 mm, right atrium ventricle is not large, left ventricular ejection fraction 58%, inferior posterior wall motion is relatively weak, the rest of the ventricular wall motion is normal, each valve morphology, structure, opening and closing motion did not see obvious abnormalities. The first consideration was that the patient had postoperative cardiac insufficiency, and the symptoms were not significantly relieved after treatment with coronary artery dilation and diuresis. In combination with the patient’s significant hypoxemia, markedly elevated D-dimer, and history of surgery and bed rest, pulmonary embolism was highly suspected, and a pulmonary vascular enhancement CT examination was performed, suggesting multiple pulmonary emboli in both lungs and bilateral pleural effusion.
Case 2, a 59-year-old male patient was admitted to the hospital with chest tightness and shortness of breath after activity for 2 years and right lower limb edema for 1 month. 2 years ago, he was diagnosed with dilated cardiomyopathy by echocardiography after activity due to shortness of breath and weakness, and his symptoms improved after symptomatic treatment. The edema of the right lower limb did not subside significantly. On examination after admission: BP: 120/85 mmHg, clear breath sounds in both lungs, no dry and wet rales, HR 70 beats/min, rhythmical, grade 2 systolic murmur heard in the apical region, right lower limb edema. Arterial blood gas analysis: pH 7.45, PO2 88.3 mmHg, PCO2 40.3 mmHg, HCO3- 27.5 mmol/L. D-dimer 3.59 μg/ml. Chest X-ray: heavy texture in both lungs, enlarged heart, cardiothoracic ratio 0.7. ECG: atrial fibrillation, ST-T changes. Echocardiogram: left atrium 50 mm, left ventricle 80 mm end-diastolic intra-ventricular meridian, right ventricle 37 mm, left ventricular ejection fraction 30%, whole heart enlargement, mainly in the left ventricle, normal wall thickness, diffusely reduced systolic amplitude, estimated pulmonary artery high systolic pressure 50 mmHg, enlarged mitral annulus, poor valve closure, tricuspid regurgitation. After admission, considering that the patient’s symptoms did not improve significantly when treated for exacerbation of cardiac insufficiency and there was only right lower extremity edema, right lower extremity deep vein thrombosis was firstly suspected. He was immediately treated with low-molecular-weight heparin and warfarin anticoagulation on the basis of dilated cardiomyopathy, and the symptoms resolved and the right lower extremity edema subsided significantly after 1 week.
Discussion
Symptoms such as chest tightness and shortness of breath that occur in left heart disease with pulmonary embolism are generally thought of first as a problem of the left heart disease itself, and rarely consider the occurrence of pulmonary embolism. The first patient was an elderly male with chest tightness, shortness of breath, and intermittent fever after coronary artery bypass grafting. The clinician first considered the patient’s postoperative cardiac insufficiency and infection, but the patient’s postoperative echocardiography suggested that the systolic function of the heart was basically normal, was it diastolic insufficiency? Even if the latter is the case, the patient’s symptoms should improve quickly after diuretic treatment, but the patient’s symptoms did not ease after coronary artery dilation and diuretic treatment. Arterial blood gas and D-dimer were immediately checked, suggesting significant hypoxemia and elevated D-dimer levels. Combined with the patient’s surgical and ambulatory history, pulmonary embolism was highly suspected, and pulmonary vascular enhancement CT examination then confirmed multiple pulmonary embolisms. Subsequent anticoagulation therapy resulted in significant relief of the patient’s symptoms and return to normal body temperature, so the patient’s intermittent postoperative hypothermia was likely thrombus resorption fever. The second patient was a patient with dilated cardiomyopathy. It was easy to think of the exacerbation of left heart disease when there was chest tightness, shortness of breath and lower extremity edema, but the problem that the doctor overlooked was that the exacerbation of heart failure generally manifested as bilateral lower extremity edema, while this patient had unilateral lower extremity edema, which was not well explained by the deterioration of heart function. Unilateral lower extremity edema is the first consideration of lower extremity deep vein thrombosis. The patient’s D-dimer was significantly elevated, and the echocardiogram suggested pulmonary hypertension, which should be highly suspected clinically as pulmonary embolism. The patient achieved significant results with anticoagulation therapy based on the treatment of dilated cardiomyopathy.
Combined with the analysis of the above 2 cases, the author believes that left heart disease combined with pulmonary embolism has the following characteristics: 1. When left heart disease is accompanied by cardiac insufficiency or after surgery, the patient is bedridden and less active, and venous thrombosis is easily formed. 2. The clinical symptoms of left heart disease combined with pulmonary embolism are not easily distinguished from the aggravation of left heart disease itself. 3. The left ventricle predominates. Therefore, the electrocardiogram rarely shows the characteristic manifestations of right heart dilatation and right heart load aggravation, such as S1QIIITIII type, QRS electric axis right deviation, right bundle branch conduction block, etc. 4. When pulmonary embolism is combined with left heart disease, the echocardiographic picture is still dominated by the manifestations of the left heart disease, and the manifestations of the right heart system are not obvious. The above characteristics are also the main reason why pulmonary embolism combined with left heart disease is easily missed. I believe that if clinicians pay attention to the following points, it will help to reduce the underdiagnosis of pulmonary embolism in combination with left heart disease: 1. D-dimer is a product of cross-linked fibrin. As long as there is activated thrombosis and fibrinolytic activity in the body, D-dimer will be elevated, such as myocardial infarction, cerebral infarction, pulmonary embolism, venous thrombosis, surgery, tumor, diffuse intravascular coagulation, infection, and tissue necrosis. Since the sensitivity of D-dimer for the diagnosis of acute pulmonary embolism is as high as 92%-98%, while the specificity is only 40%-43%, it has a greater diagnostic value for the exclusion of acute pulmonary embolism, and if its content is lower than 500 μg/L, acute pulmonary embolism can be basically excluded. 5. Raise awareness of the diagnosis of deep vein thrombosis (DVT) Clinicians should not neglect the consultation and examination of patients with lower extremity venous disease, carefully inquire about the susceptibility factors of DVT, previous history of venous thrombosis, lower extremity pain and swelling symptoms, etc., and check the lower extremity skin color, lower extremity circumference, superficial varicose veins, etc. 6. The ECG and/or echocardiographic manifestations of a few patients with left heart disease cannot be explained by left heart disease itself.