Electrocardiogram Demonstrated Sinus Rhythm Research Articles

P881 Young patient with left ventricular hypertrophy and accidentally discovered aortic dissection: hypertensive heart or hypertrophic cardiomyopathy?

Abstract A 36-year-old male with positive family history of sudden cardiac death (his uncle"s son died suddenly at the age of 25), hospitalized a month ago in a local hospital due to acute hypertensive cardiogenic pulmonary edema, was referred to our institution for further evaluation with suspicion of hypertrophic cardiomyopathy. On admission patient was asymptomatic, without fatigue, exertional dyspnoea, chest pain or syncope. On physical examination his BP was significantly elevated (180/100 mmHg). The lungs were clear on auscultation, liver was not enlarged, jugular veins were normal, there was no oedema of lower extremities. Abdominal auscultation revealed vascular murmur in umbilical region. The baseline level of NT-proBNP was 811.4 (range 0–125) pg/mL, and high-sensitivity cardiac troponin T was 20.2 (range 0–14) ng/L. The standard 12-lead electrocardiogram demonstrated sinus rhythm, left atrial enlargement and left ventricular (LV) hypertrophy with nonspecific ST segment and T-wave changes (Fig. 1A). No significant pathology was present on chest X-ray (Fig. 1B). Transthoracic echocardiography revealed significant concentric LV hypertrophy with preserved LV ejection fraction (EF 70%) and moderately decreased global longitudinal strain (GLS-13.7%). There was mild dilatation of left atrium. Ascending aorta diameter was in normal range (Fig. 1C-D). Cardiac magnetic resonance (CMR) scan confirmed concentric LV hypertrophy with the maximal wall thickness of 18 mm at interventricular septum, and increased myocardial mass (LV mass index 124 ml/m2, range 59–92). Moreover, small areas of late gadolinium enhancement were found in LV segments (Fig. 1E-F). Due to presence of vascular murmur in abdomen, ultrasound imaging was performed. The exam revealed abdominal aortic dissection (Fig. 1G-H). Patient was transferred to the computed tomography (CT) unit to confirm the diagnosis. Aortic dissection originated below renal arteries and involving common illiac arteries was detected (Stanford B). The presence of thrombi within the lumen created by the aortic dissection suggested chronic presentation. Patient was managed conservatively with strict blood pressure control and close follow up arranged. We decided to perform genetic analysis. Currently we are awaiting the results in hope that it will help us to establish the diagnosis and differentiate hypertensive heart from hypertrophic cardiomyopathy. In conclusion, aortic dissection typically presents with tearing chest pain and severe hemodynamic compromise. Painless dissection, like in this case, is relatively rare. Differential diagnosis between hypertensive heart and hypertrophic cardiomyopathy is crucial as it has direct therapeutic impact. Abstract P881 Figure 1

P1253 A case report of acromegalic cardiomyopathy with severe left ventricular hypertrophy

Abstract Introduction Acromegaly is a rare disease, mostly caused by a growth hormone (GH)-secreting benign pituitary tumor, with an increased production of GH and insulin-like growth factor 1 (IGF-1). One hallmark feature of the disease is acromegalic cardiomyopathy, a syndrome of progressive cardiac dysfunction characterized by left ventricular hypertrophy, diastolic dysfunction, and combined systolic and diastolic dysfunction in the very advanced stage. Clinical case A 54-year-old male with history of arterial hypertension and abnormal electrocardiogram (ECG) for more than 10 years was diagnosed with active stage of acromegaly (IGF-1-1711ng/ml, cardiac magnetic resonance (CMR) – pituitary tumor). Surgical treatment was recommended. He was referred for preoperative cardiac evaluation preceding transsphenoidal resection of a pituitary adenoma. He denied syncope or any chest pain. The standard 12-lead ECG demonstrated sinus rhythm, left atrial enlargement and left ventricular (LV) hypertrophy with deep negative T waves in V3-V6 leads. Holter monitor demonstrated episodes of non-sustained ventricular tachycardia. Transthoracic echocardiography revealed severe asymmetric LV hypertrophy without LVOT obstruction at rest and maneuver Valsalva (max. grad. – 19mm. Hg) with mildly abnormal LV ejection fraction (48%, range ≥52%), severe reduced global longitudinal strain (-8,2%, range <-18%) and grade II diastolic dysfunction. CMR imaging was performed. According to CMR suggested hypertrophic cardiomyopathy (HCM) demonstrating area of myocardial fibrosis on extensive late gadolinium enhancement, maximal LV wall thickness of 40 mm, increased myocardial mass (index 277g/m2, range 68–103g/m2) and mildly reduced systolic LV function (LVEF - 54%, range 57-74%). Coronary angiography did not show significant stenosis. After cardiac examination, transsphenoidal adenomectomy was done. There are currently no algorithms sudden cardiac death (SCD) for patients with acromegalic cardiomyopathy, but he was recommended implantation of cardioverter defibrillator devices on a scale for HCM (Risc SCD – 4,17%). Acromegaly-induced cardiomyopathy can mimic HCM. He was also recommended genetic typing for HCM, considering the results of MRI. Conclusion/Discussion: Reduction GLS might be expected to result in a fall in LVEF, however this is often not the case in hypertrophic LV diseases. It is important to note that measures of regional function such as myocardial strain may actually reflect global systolic function better than the ejection fraction. The results may improve our ability to provide a more accurate prognosis and better assessment of actual systolic function. Because cardiomyopathy is an important cause of mortality in acromegaly, diagnosis and appropriate management are critical to improve survival. Abstract P1253 Figure.

Loperamide-Induced Torsades de Pointes: A Case Series

BackgroundLoperamide is an over-the-counter, inexpensive, antidiarrheal opioid that can produce life-threatening toxicity at high concentrations. Case Report 1A 28-year-old man with a history of depression and substance abuse disorder (SUD) presented to the emergency department (ED) with shortness of breath and lightheadedness. He ingested large amounts of loperamide daily. The patient's initial electrocardiogram (ECG) demonstrated sinus rhythm, right axis deviation, undetectable PR interval, QRS 168 ms, and QTc 693 ms. He was administered intravenous sodium bicarbonate and magnesium sulfate and admitted to the intensive care unit, eventually developing Torsades de Pointes (TdP). He was given lidocaine and isoproterenol infusions, and an external pacemaker was placed. He was discharged in stable condition on hospital day (HD) 16. Case Report 2A 39-year-old woman with a history of hepatitis C, depression, and SUD was transported to the ED after reported seizure-like activity. The patient experienced TdP in the ED and admitted to ingesting large amount of loperamide daily. An ECG demonstrated sinus rhythm, right axis deviation, PR interval 208 ms, QRS interval 142 ms, and QTc 687 ms. She was administered intravenous magnesium, sodium bicarbonate, and isoproterenol. After intensive care unit admission, the patient experienced no further TdP and was discharged on HD 6. Why Should an Emergency Physician Be Aware of This?Emergency physicians should proceed with caution when treating patients with loperamide toxicity. Even in asymptomatic patients and drug discontinuance, obtain consultation with a medical toxicologist, promptly treat ECG abnormalities aggressively, and admit all patients for further monitoring.

Focal Takotsubo Cardiomyopathy- Insights from Cardiac MRI Imaging

Case: A previously well 62-year-old female presented to the emergency department with central chest pain following an argument. Initial electrocardiogram demonstrated sinus rhythm with ST-elevation in V1-V2. She underwent emergent coronary angiography which demonstrated no obstructive coronary artery stenosis. Left ventriculography demonstrated focal dyskinesis of the mid anterior left ventricular (LV) wall. Contrast enhanced transthoracic echocardiography (TTE) confirmed the appearance and demonstrated a pericardial effusion, raising the suspicion of a contained LV rupture. Cardiac magnetic resonance (CMR) imaging confirmed the presence of an anterior wall aneurysm with associated oedema on T2 weighted images (Fig. 1) however there was no evidence of associated late gadolinium enhancement (LGE) in the region (Fig. 1). The findings were thought to be most consistent with a focal Takotsubo cardiomyopathy (TC). Repeat TTE 1 month later demonstrated complete normalisation of LV contraction. Discussion: TC is a rare syndrome characterised by transient regional systolic dysfunction of the LV, mimicking myocardial infarction, but in the absence of angiographic evidence of obstructive coronary artery disease or acute plaque rupture. Focal involvement of the myocardium is its rarest form. A large multi-centre study in this population found CMR can accurately identify TC through a typical pattern of LV dysfunction and demonstrates myocardial oedema in 81% patients, and no significant LGE in 91%.

Validation of PR interval length as a criterion for development of atrial fibrillation in non-Hispanic whites, African Americans and Hispanics

BackgroundPR interval prolongation on electrocardiogram (ECG) increases the risk of atrial fibrillation (AF). Non-Hispanic Whites are at higher risk of AF compared to African Americans and Hispanics. However, it remains unknown if prolongation of the PR interval for the development of AF varies by race/ethnicity. Therefore, we determined whether race affects the PR interval length's ability to predict AF and if the commonly used criterion of 200 ms in AF prediction models can continue to be used for non-White cohorts. MethodsThis is a retrospective epidemiological study of consecutive inpatient and outpatients. An ECG database was initially interrogated. Patients were included if their initial ECG demonstrated sinus rhythm and had two or more electrocardiograms and declared a race and/or ethnicity as non-Hispanic White, African American or Hispanic. Development of AF was stratified by race/ethnicity along varying PR intervals. Cox models controlled for age, gender, race/ethnicity, systolic blood pressure, BMI, QRS, QTc, heart rate, murmur, treatment for hypertension, heart failure and use of AV nodal blocking agents to assess PR interval's predictive ability for development of AF. Results50,870 patients met inclusion criteria of which 5,199 developed AF over 3.72 mean years of follow-up. When the PR interval was separated by quantile, prolongation of the PR interval to predict AF first became significant in Hispanic and African Americans at the 92.5th quantile of 196–201 ms (HR: 1.42, 95% CI: 1.09–1.86, p=0.01; HR: 1.32, 95% CI: 1.07–1.64, p=0.01, respectively) then in non-Hispanic Whites at the 95th quantile at 203–212 ms (HR: 1.24, 95% CI: 1.24–1.53, p=0.04). For those with a PR interval above 200 ms, African Americans had a lower risk than non-Hispanic Whites to develop AF (HR: 0.80, 95% CI: 0.64–0.95, p=0.012), however, no significant difference was demonstrated in Hispanics. ConclusionsThis is the first study to validate a PR interval value of 200 ms as a criterion in African Americans and Hispanics for the development of AF. However, a value of 200 ms may be less sensitive as a predictive measure for the development of AF in African Americans compared to non-Hispanic Whites.

IS ST-SEGMENT DEPRESSION EQUIVALENT TO ST-SEGMENT ELEVATION IN PATIENTS PRESENTING WITH OUT-OF-HOSPITAL CARDIAC ARREST?

Following an out-of-hospital cardiac arrest (OHCA), systematic post-arrest care improves the likelihood of survival and neurological recovery. The immediate post resuscitation 12-lead electrocardiogram (ECG) aids in the diagnosis of an acute coronary syndrome (ACS); this can occur in up to 50% of adults presenting with OHCA. We aimed to characterize the relationship between the post-resuscitation ECG and coronary angiography (CA) during the index admission. A retrospective chart review of consecutive adult patients admitted to St. Paul’s and Mt. St. Joseph’s Hospitals following an OHCA, between January 2010 and December 2011, was undertaken. Patients were identified using the Resuscitation Outcomes Consortium Cardiac Arrest Epistry databases and included if they were admitted to hospital and had interpretable post-resuscitation ECG. ST-segment changes of >0.1mV in two contiguous leads were considered significant. A stenosis of >70% was classified as obstructive coronary artery disease (CAD) and >50% for left main stenosis. Coronary occlusion was defined as >99% stenosis. Our cohort consisted of n=65 patients with a mean age of 62 ± 17 years and 69% were male. The initial rhythm on paramedic arrival was ventricular tachycardia/fibrillation (n=29; 45%), asystole (n=15; 23%), pulseless electrical activity (n=8; 12%), and unspecified (n=13; 20%). The post-resuscitation ECG demonstrated sinus rhythm (n=44; 68%), atrial tachycardia (n=13; 20%), and other (n=8; 12%). The median heart rate was 95bpm (IQR=72-114bpm), QRS duration 112ms (IQR=94-146ms), and corrected QT interval 456ms (IQR=415-494ms). The QRS morphology included narrow complex (n=35; 54%), non-specific intraventricular conduction delay (n=11; 17%), RBBB (n=14; 22%), and LBBB (n=5; 8%). The rate of CA was 42% (n=27). The table below shows CA findings stratified by ST segment change. At CA the mean LVEDP was 20mmHg and LVEF was 41%. The odds ratios (OR) of coronary occlusion for ST-elevation was 21.6 (95% CI=2.1-218.6; p=0.002) and for non ST segment change was 0.07 (95% CI=0.01 - 0.5; p=0.004). In patients with ST-depression there was a trend towards coronary occlusion (OR 4.5 95% CI=0.5-41.2; p=0.17). A significant proportion of patients presenting with OHCA demonstrated ST-segment changes on the post-resuscitation ECG. Rates of coronary angiography in OHCA patients were low. The findings of significant CAD were frequent, irrespective of ST-segment shift. The presence of ST- depression showed a trend towards coronary occlusion. Systematic evaluation of patients with ST depression is warranted to further improve survival and neurological recovery post OHCA.

Diagnosis of Cardiac Amyloidosis by Skin Lesions

In June 2011, a 74-year-old man was admitted for recurrent heart failure. He had hypertension, diabetes mellitus, renal failure due to nephrosclerosis and diabetic nephropathy, prostate cancer, tuberculosis, and gouty arthritis, and had received a parathyroidectomy. In 2009, he had received a mechanical prosthesis to treat aortic stenosis. Cardiac auscultation was rhythmic, with no murmurs, and with normal prosthetic sounds. The patient presented petechiae, purpura, papules, and spontaneous ecchymosis at the eyelids, groin, neck, and axillas (Figure 1), with onset after initiation of acenocoumarol in 2009. The electrocardiogram demonstrated sinus rhythm with a long P-R interval, right bundle branch block with left anterior hemiblock, and low voltage, consistent with infiltrative cardiomyopathy (Figure 2). The echocardiogram demonstrated left ventricular hypertrophy with increased echogenicity (Figures 3A and B), ejection fraction of 45%, and a restrictive pattern on pulsed Doppler (Figure 3C: increased E/A ratio) and tissue Doppler (Figure 3D: decreased E’ and A’ peaks). Examination of skin biopsy specimens with Congo red stain showed amyloidosis secondary to monoclonal gammopathy, with positive immunohistochemistry for lambda light chains. He was treated with melphalan and dexamethasone, which were discontinued because of a favorable hematological response, with normalization of serum free light chain concentrations. Thereafter, he was hospitalized several times for heart failure and ultimately died of this cause in 2013. The purpura, petechiae, and ecchymosis were due to intracutaneous bleeding, resulting from a fragile vascular status secondary to amyloid infiltration. This is sometimes the first and only sign of systemic amyloidosis. Although these features are not specific to this disease, they may be an aid to its diagnosis and prompt treatment in the appropriate clinical context. Figure 3. Figure 1. I

Acquired Fontan Physiology Secondary to Acute Mechanical Tricuspid Valve Failure in a Patient With Massive Right Heart Enlargement and Ebstein’s Anomaly

A 25-year-old man with Ebstein’s anomaly and a secundum atrial septal defect had a mechanical tricuspid valve replacement (St. Jude 31-mm valve) and atrial septal defect closure when he was 15 years old. He was under long-term specialist follow-up and had recently been admitted with symptoms and signs of right heart failure secondary to new onset atrial flutter. He was direct-current cardioverted and commenced on ramipril and metoprolol. He then went to have an electrophysiological study and successful atrial flutter ablation. At review 6 months later he reported good exercise tolerance and was now able to play 18 holes of golf, whereas previously he could only manage 9 holes. However, he commented that since the electrophysiological procedure he had been unable to hear his prosthetic valve clicks. On clinical examination he was not cyanosed, the jugular venous pressure was elevated at 4 cm without prominent V waves, there was a soft first heart sound, no audible mechanical valve clicks, and a pansystolic murmur. There were no signs of heart failure or peripheral edema. An electrocardiogram demonstrated sinus rhythm, right axis deviation, first-degree heart block, and right bundle-branch block with QRS duration of 200 ms. Echocardiography and fluoroscopy (Figure 1) showed that the leaflets of the …

Large hiatal hernia at chest radiography in a woman with cardiorespiratory symptoms

Hiatal hernia (HH) is a frequent entity. Rarely, it may exert a wide spectrum of clinical presentations mimicking acute cardiovascular events such as angina-like chest pain until manifestations of cardiac compression that can include postprandial syncope, exercise intolerance, respiratory function, recurrent acute heart failure, and hemodynamic collapse. A 69-year-old woman presented to the emergency department complaining of fatigue on exertion, cough, and episodes of restrosternal pain with less than 1 hour of duration. Her medical history only included some episodes of bronchitis and no history of hypertension. The 12-lead electrocardiogram demonstrated sinus rhythm with right bundle-branch block. Laboratory tests, including cardiac troponin I, were within normal reference values. Chest radiography showed no significant pulmonary alterations and revealed in mediastinum a huge abnormal shadow overlapping the right heart compatible with a gastric bubble.The gastroscopy confirmed a large HH. A 2-dimensional transthoracic echocardiogram, using all standard and modified apical and parasternal views, revealed an echolucent mass, compatible with HH, compressing the right atrium. Also, it showed an altered left ventricular relaxation and a mild increase of pulmonary artery pressure (35 mm Hg). Spirometry showed a mild obstruction of the small airways, whereas coronary angiography showed normal coronary arteries. We concluded that the patient's symptomatology was related to the compressive effects of the large hiatal ernia, a neglected cause of cardiorespiratory symptoms. The surgical repair of HH was indicated.

A rare case of massive papillary fibroelastoma of the right ventricular free wall

A 51-year-old previously healthy woman was referred to our institution with atypical chest pain. Physical examination and laboratory findings were normal. The electrocardiogram demonstrated sinus rhythm of 70 beats/min with a right bundle branch block. Routine chest X-ray showed calcifications projecting on the heart. Transthoracic echocardiography was hampered by a limited acoustic window. Cardiovascular magnetic resonance revealed a well-demarcated mass in the right ventricle in conjunction with the right ventricular free wall (Fig. 1). Dimensions were 9.5 × 4.5 × 4.5 cm. Computed tomography of the thorax demonstrated a densely calcified mass located in the right ventricle but showed no evidence of pulmonary embolism or intrapulmonary masses (Fig. 2a and b). Finally, transvenous biopsy of the tumour led to the histological diagnosis of papillary fibroelastoma (Fig. 2d). To our knowledge, this is the first well-documented case of a large calcified papillary fibroelastoma of the right ventricular free wall [1, 2]. Fig. 1 Cardiovascular magnetic resonance (CMR) demonstrates a large mass in the right ventricle in conjunction with the right ventricular free wall. On cine-imaging, the mass exhibited a somewhat lower signal than the left ventricular myocardium (a and b). T1 ... Fig 2 Axial (a) and (b) coronal CT image show a large and heavily calcified mass at the right ventricular free wall. Coronary angiography (c) shows a large non vascularised calcified mass. Histological examination (d) in haematoxylin and eosin stain reveals ...

Atrioventricular Valve Dyssynchrony Resulting From Severe Mitral Regurgitation

A nearly 4-year-old Ethiopian girl with a 1-year history of weight loss and rapid breathing who had just immigrated to the United States presented to the emergency department with respiratory distress and increasing lethargy. Over the preceding year, she had been found to have increasing tachypnea, anorexia, a 5-kilogram weight loss, fatigue, intermittent emesis, and decreased urine output. There were multiple notable findings on the physical examination. Abnormalities of the vital signs included a respiratory rate of 52 breaths per minute, blood pressure of 70/53, and an oxygen saturation of 85% on room air. In general, she was cachectic and lethargic. There was jugular venous distension with accentuated a waves. There were diffuse fine inspiratory crackles across the lung fields. There was asymmetrical protrusion of the left anterior chest with a visible, dynamic cardiac impulse. On auscultation, there was a regular rhythm with an S3 present. There was a III/VI, holosystolic, midfrequency, blowing murmur in the 5th intercostal space at the midclavicular line with radiation to the apex and the left axilla. A diastolic rumble was not appreciated. The liver edge was 4 centimeters below the right costal margin. Pulses were normal at the brachia and femoral arteries, bilaterally. There was no peripheral edema or clubbing. Blood work revealed a negative troponin and a B natriuretic peptide of 2761 picograms per milliliter. A chest radiograph was performed, which showed cardiomegaly with enlargement of the left superior cardiac border, bilateral pulmonary edema, and superior deviation of the left mainstem bronchus suggestive of left atrial dilatation (Figure 1). A 15-lead electrocardiogram demonstrated sinus rhythm with left atrial enlargement and ST segment elevation in the anterior precordial leads (Figure 2). Figure 1. A chest radiograph taken in an anteroposterior projection demonstrates: pronounced cardiomegaly with a cardiothoracic ratio of 71%; a double contour of …

Multimodality cardiac magnetic resonance imaging of cardiac mass

An 84-year-old man presented with a 1-month history of dyspnoea and constrictive chest pain on exertion, relieved by nitroglycerin administration. His main medical history included aortic valve replacement (AVR) with a bioprosthetic valve, coronary artery bypass graft (CABG) and post-transfusion chronic hepatitis C. Physical examination was normal except for a grade 2 ejection systolic murmur audible in the aortic area and bilateral leg oedema. Electrocardiogram demonstrated sinus rhythm at 75/min and T-wave inversion in the inferior leads. Moderately elevated troponin concentration was noted (0.79 g/L). The patient was transferred to the intensive care unit with a preliminary diagnosis of acute coronary syndrome. Transthoracic echocardiography (TTE) revealed a hyperechogenic and heterogeneous motionless mass infiltrating the lateral wall of the right ventricle and atrium (Fig. 1, Panel A, black arrow) without intracavitary extension. Left ventricular ejection fraction was normal.

A Case with Patent Ductus Arteriosus Complicated by Pulmonary Artery Endarteritis

Case A 49-year-old woman, with no history of heart disease, was admitted to the hospital with a febrile sensation, fatigue, and weight loss (2 kg). Three months ago, she was diagnosed as having a stricture of the pulmonary artery and suspicious pneumonia. So, the patient was treated empirically with antibiotics at another hospital. However the symptoms did not improve. No further information was obtained from the past medical and family history. On physical examination, the blood pressure was 130/80 mmHg, the heart rate was 68 beats/min and regular, and the body temperature was 38。C. On inspection, the conjunctivae were anemic. Cardiac auscultation revealed a continuous murmur (grade III) at the left parasternal border. Laboratory investigations revealed a normocystic, normochromic anemia (Hemoglobin 9.66 g/dL). The white cell count, C-reactive protein and erythrocyte sedimentation rate were 5,960×10/L, 6.52 mg/dL and 21 mm/h, respectively. The renal and liver function tests were normal. The chest X-ray revealed cardiomegaly (C/T ratio=0.6). The chest CT showed a dilated pulmonary artery and thombus in the proximal side of left main pulmonary artery. An electrocardiogram demonstrated sinus rhythm and the minimal voltage criteria for left ventricular hypertrophy. Transthoracic echocardiography (TTE) showed a 0.5 cm defect between the descending thoracic aorta and the main pulmonary artery and a 3.4×1.0 cm hypoechogenic movable vegetation attached to the wall of the main pulmonary artery (Fig. 1). The left atrium was enlarged (4.26 cm). However, the diameter of left ventricle was normal. TTE showed a diastolic filling pattern of impaired relaxation (E/E’=12.3). Transesophageal echocardiography (TEE) showed a 0.9 cm patent ductus arteriosus (PDA) and a left to right shunt

Cardiac resynchronization therapy for an unusual cause of cardiomyopathy

A 66 year old woman with symptomatic cardiac failure, despite treatment with diuretics, a β-blocker and an ACE inhibitor was referred for consideration of cardiac resynchronization therapy (CRT). Co-morbidity included chronic renal impairment and type II diabetes mellitus. An electrocardiogram demonstrated sinus rhythm, first degree block and left bundle branch block of 160 ms duration. Coronary angiography was normal and transthoracic 2D echocardiography showed severe left ventricular systolic dysfunction with extensive and abnormal trabeculation of the left ventricular lateral, anterior and apical segments. Significant interventricular dys-synchrony (63 ms delay in left vs. right ventricular ejection on Doppler) and intra-ventricular dyssynchrony of the left ventricle were also found (208 ms delay in posteroseptal vs. anteroseptal peak wall thickening on M-mode and with tissue Doppler a 220 ms delay of the basal lateral vs. basal septal segment peak systolic velocity). Moreover, the appearances were highly suggestive of isolated

Uterine artery embolisation for massive uterine fibroids in the presence of submassive pulmonary emboli

A 46-year-old woman was admitted to our hospital with acute shortness of breath and pre-syncope. She had known massive uterine fibroids with a history of menorrhagia and dysmenorrhoea, and had been awaiting total abdominal hysterectomy and bilateral salpingo-oophorectomy. She had no past or family history of venous thromboembolism (VTE). She was an ex-smoker with a 16-pack/year smoking history. On examination, she looked unwell, was sweaty and clammy, but apyrexial. Her heart rate was 130 per minute and her blood pressure was 140/95 mmHg. She was tachypnoeic with a respiratory rate of 28 breaths per minute; however, her chest was clear. Abdominal examination revealed an enormous uterus, equivalent to the size of a 30-week pregnancy. There was no clinical evidence of deep vein thrombosis (DVT). She was hypoxic: oxygen saturation on air was 88%; arterial blood gas measurement on 100% oxygen—pH 7.4, PO2 29.0mmHg, PCO2 3.5mmHg, bicarbonate 18.5mmol/L, base excess of 7.5 mol/L. Her full blood count revealed a microcytic anaemia with a mean cellular volume of 67.9 fl (normal: 81–99 fl) and haemoglobin of 9.4 g/dL (normal: 12.0–15.0 g/L). Her D-dimer was significantly elevated at 1.7 Ag/mL (normal: <0.5 Ag/mL). Other blood tests including renal profile, liver function, thyroid function, C-reactive protein and clotting profile were all within normal limits. Her 12 lead electrocardiogram demonstrated sinus rhythm with right bundle branch block and T wave inversion in V1-3 with classic ‘S1QIIITIII’ changes. Her Chest X-ray showed blunting of the basal pulmonary arteries particularly on the right. Transthoracic echocardiography findings were consistent with submassive pulmonary embolism: the left ventricular size and function was normal; the right ventricle was dilated with moderately impaired systolic function; the right atrium was also dilated; the inferior vena cava was distended and failed to collapsewith inspiration; the estimated right ventricular systolic pressure was 50 mmHg. A contrast CT pulmonary angiogram revealed occlusive thrombus in the proximal basal left and mid and basal right pulmonary arteries. She was initially managed with aggressive fluid resuscitation and was commenced on intravenous unfractionated heparin (target APTT ratio of 2.0–3.0). On day 3 she began to heavily menstruate and required a total of nine units of blood over the ensuing 10 days. She was given subcutaneous Zoladex and 30 mg TDS provera to reduce her menstrual blood loss. On day 13 she underwent iliac venography and inferior cavography with insertion of a temporary IVC filter. No free intravascular thrombus was seen in either common iliac vein or within the IVC. There was however significant compression on all three of these veins. Immediately following this, she underwent uterine artery embolisation (UAE). At the time of UAE, her uterus and dominant fibroid measured 3800 and 3220 mL, respectively. Two weeks post-UAE her caval filter was removed, via a jugular route, without complication. A follow up pelvic MRI, one month later, confirmed complete fibroid degeneration with migration of the fibroid into the endometrial cavity (Fig. 1). The uterus measured 2200 mL and the fibroid 1000 mL, correlating with a 42% and 69% respective relative reduction in size. At six weeks she passed a large ‘steak-sized’ degenerate fibroid. At three months pelvic ultrasound showed that the uterus had reduced to 315 mL and the fibroid volume was 1.5 mL. The patient has made a complete recovery and has been given life-long warfarin.