Medical Image of the Week: Type A Aortic Dissection Extending Into Main Coronary Artery

Figure 1. Electrocardiogram at presentation showing ST segment elevation in anterior leads (arrows).

Figure 2. Coronary angiogram showing RAO caudal view of left main coronary artery after contrast injection with the smooth proximal linear irregularity suspicious for dissection flap into the left anterior descending artery (arrow).

Figure 3. Panel A: Computed tomography angiogram transverse view showing true lumen and false lumen of both ascending and descending aorta (arrow). Panel B: Computed tomography angiogram sagittal view showing dissection from root into abdominal aorta. 

A 58-year-old woman with no significant past medical history, presented to the emergency department with complains of sudden onset, severe , non-radiating epigastric pain associated with nausea and vomiting. An electrocardiogram (EKG) done in emergency department showed ST segment elevation in the anterior leads (Figure 1). Blood pressure at presentation was 141/79, and she had symmetrical bilateral pulses of the upper extremities, no diastolic murmur, and no neurologic deficit. The patient was taken to catherization laboratory, for ST segment elevated myocardial infarction (STEMI). She was found have aortic dissection extending to the left main coronary artery (Figure 2). Cardiothoracic surgery was called immediately. Computed tomography angiogram (CTA) of the thoracic and abdominal aorta revealed Debakey type 1 aortic dissection. (Figure 3). The patient was taken to the operating room. Unfortunately, the patient suffered pulseless electrical activity (PEA) arrest during anesthesia induction from which she could not be revived.

Aortic dissection is a critical compromise in the lining of the main arterial outflow from the heart (1).  Two theories have been proposed to explain the pathogenesis. A tear in the tunica intima, of the aorta, leads to blood from the aortic lumen surging into the tunica media (2). In contrast, the second theory holds that the vasa vasorum in the more outer portions of the tunica media hemorrhage first and then cause the rupture of the tunica intima (2). The pressure of the pulsatile blood flow extends the dissection, typically in an anterograde fashion (2). Anatomically aortic dissection is classified as Debakey 1,2, and 3 and Stanford A and B (1). Rarely aortic dissections can also extend in a retrograde fashion to reach the coronary ostia (3). Signs of myocardial ischemia including ST segment changes, adversely affect survival outcomes in patients with type A aortic dissection extending to the coronary arteries (4).

Ali Osama Malik MD¹, Oliver Abela MD², Chowdhury Ahsan MD², and Jimmy Diep MD²

¹Department of Internal Medicine

²Department of Cardiovascular Medicine

University of Nevada School of Medicine

Las Vegas, NV USA

References

1. Golledge J, Eagle KA. Acute aortic dissection. Lancet. 2008 Jul 5;372(9632):55-66. [CrossRef] [PubMed]
2. Patel AY, Eagle KA, Vaishnava P. Acute type B aortic dissection: insights from the International Registry of Acute Aortic Dissection. Ann Cardiothorac Surg. 2014 Jul;3(4):368-74. [CrossRef] [PubMed]
3. Neri E, Toscano T, Papalia U, Frati G, Massetti M, Capannini G, et al. Proximal aortic dissection with coronary malperfusion: presentation, management, and outcome. J Thorac Cardiovasc Surg. 2001 Mar;121(3):552-60. [CrossRef] [PubMed]
4. Imoto K, Uchida K, Karube N, Yasutsune T, Cho T, Kimura K, et al. Risk analysis and improvement of strategies in patients who have acute type A aortic dissection with coronary artery dissection. Eur J Cardiothorac Surg. Sep;44(3):419-24; discussion 24-5. [CrossRef] [PubMed]

Cite as: Malik AO, Abela O, Ahsan C, Diep J. Medical image of the week: type A aortic dissection extending into main coronary artery. Southwest J Pulm Crit Care. 2017;14(5):238-9. doi: https://doi.org/10.13175/swjpcc044-17 PDF 

Medical Image of the Week: Wolff-Parkinson-White Syndrome

Figure 1. Presenting EKG with supraventricular tachycardia at rate of 232.

Figure 2. Post-conversion EKG demonstrating a short PR interval, slurring of the initial QRS upslope (delta wave), widened QRS, and ST-T repolarization change; characteristic of Wolff-Parkinson-White Syndrome.

A 38-year-old man developed sustained rapid heart rate while rock climbing. The patient reported that he had experienced rare bouts of self-limited palpitations in the past. Blood pressure on arrival to the emergency department was 112/ 65 mm Hg. The patient’s initial EKG demonstrated a regular, narrow complex supraventricular tachycardia, with a rate of 232 (Figure 1). Intravenous adenosine was administered with no change in his rate or rhythm. The patient then received amiodarone by intravenous bolus, with subsequent conversion to sinus rhythm (Figure 2).

Wolff-Parkinson-White (WPW) syndrome is a congenital cardiac condition present in approximately 0.15% of the general population. WPW is characterized by the abnormal presence of conduction tissue that creates an accessory atrioventricular pathway and thus potentiates reentrant tachycardia (1). The classic resting EKG findings in WPW are: a shortened PR interval (less than 0.12 seconds), an indistinct initial upslope of the QRS complex (known as the delta wave), a widened QRS complex (0.12 seconds or greater), and ST-T repolarization changes (2). In WPW presenting as a narrow complex tachycardia without hypotension, the initial treatment is adenosine or a calcium channel blocker, followed by amiodarone if unsuccessful. If the presenting rhythm is atrial fibrillation, atrial flutter, or an undefined wide complex tachycardia without hypotension, amiodarone is used. A hemodynamically unstable rhythm warrants immediate electrical cardioversion. Definitive evaluation and treatment of WPW requires electrophysiologic mapping and subsequent ablation of the accessory pathway.

Charles Van Hook MD, Cristina Demian MD, Douglas Tangel MD, Jennifer Blair MD, and Lisa Patel MD

Avista Adventist Hospital

Louisville, Colorado USA

References

1. Katritsis DG, Camm AJ. Atrioventricular nodal reentrant tachycardia. Circulation. 2010 Aug 24;122(8):831-40. [CrossRef] [PubMed]
2. Mark DG, Brady WJ, Pines JM. Preexcitation syndromes: diagnostic consideration in the ED. Am J Emerg Med. 2009 Sep;27(7):878-88. [CrossRef] [PubMed]
3. Khairy P, Van Hare GF, Balaji S, et al. PACES/HRS expert consensus statement on the recognition and management of arrhythmias in adult congenital heart disease. Heart Rhythm. 2014 Oct;11(10):e102-65. [CrossRef] [PubMed]

Cite as: Van Hook C, Demian C, Tangel D, Blair J, Patel L. Medical image of the week: Wolff-Parkinson-White syndrome. Southwest J Pulm Crit Care. 2017;14(4):164-5. doi: https://doi.org/10.13175/swjpcc046-17 PDF 

Medical Image of the Week: ECG in PE

Figure 1. ECG on presentation demonstrating sinus tachycardia, anterior precordial T wave inversions and S1Q3T3, classic ECG findings of pulmonary embolism.

Figure 2. Panel A: CT angiogram demonstrating bilateral pulmonary embolism involving nearly every segmental and subsegmental pulmonary artery. Panel B: Echocardiogram, apical 4-chamber view, with dilated right ventricle and poor function. Panel C: Right leg ultrasound showing acute, non-occlusive thrombus; the right side of the image demonstrates incompressibility of the right femoral vein.

A 44-year-old male long distance truck driver with no known medical history presented with intermittent episodes of dyspnea for the past 24 hours, and an episode of exertional syncope just prior to hospitalization. The patient complained of sharp severe chest pain and reports several week history of right leg swelling. Initial Electrocardiogram (ECG, Figure 1) shows sinus tachycardia and signs of right ventricular strain with an associated troponin elevation. CT pulmonary angiography confirmed bilateral, extensive pulmonary emboli (PE) (Figure 2A, arrow at left pulmonary artery embolus). An echocardiogram showed severe right ventricular systolic dysfunction (Figure 2B, arrow indicated RV). Duplex ultrasound of the right leg showed extensive, acute, non-occlusive thrombus (Figure 2C, arrow indicates clot failing to compress). The patient received an IVC filter due to substantial clot burden. A hypercoagulability workup was negative.

The ECG is part of the typical evaluation for syncope, chest pain and shortness of breath. Multiple studies evaluating the utility of the ECG in the diagnosis of PE have been conducted (1-3). One study in patients with suspected PE undergoing diagnostic testing found that only tachycardia and incomplete right bundle branch block were significantly more prevalent in patients with PE than those without. Another study found a 39% rate of sinus tachycardia in those ultimately found to have PE compared to 24% in those who had negative studies. The S1Q3T3 phenomenon was present in 12% of those with PE vs 3% in those without. One or more traditional findings of right ventricular strain: S1Q3T3, right bundle branch block, or right axis deviation was present in only 13% of patients with PE who had RV dilation on echocardiography, however these findings were also present in 8.8% of patients with PE without evidence of RV dysfunction. Non-specific ECG findings such as sinus tachycardia and ST-T changes are the most commonly identified ECG abnormalities in patients with PE. Overall the ECG as a test for PE exhibits poor test characteristics and thus has little clinical utility for its diagnosis, despite the frequent emphasis on these findings in medical education.

Our patient’s ECG demonstrates several classic findings suggestive of PE including sinus tachycardia, S1Q3T3, and T-wave inversions in the anterior precordial leads. While certain ECG findings do correlate with the presence of PE they are frequently present in patients without PE and absent in those with the disease. ECG may have some utility in risk stratification by identifying signs of right heart strain, however echocardiography is the preferred modality.

Taylor Shekell MD², Cameron Hypes MD MPH^1,2, Yuval Raz MD¹

¹ Department of Medicine, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine

² Department of Emergency Medicine

University of Arizona Medical Center

Tucson, AZ

References

1. Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P, Wells PS. Diagnostic value of the electrocardiogram in suspected pulmonary embolism. Am J Cardiol. 2000;86:807-9. [CrossRef] [PubMed]
2. Sinha N, Yalamanchili K, Sukhija R, Aronow WS, Fleisher AG, Maguire GP, Lehrman SG. Role of the 12-lead electrocardiogram in diagnosing pulmonary embolism. Cardiol Rev. 2005;13:46-9. [PubMed]
3. Stein P, Matta F, Sabra M, et al. Relation of electrocardiographic changes in pulmonary embolism to right ventricular enlargement. Am J Cardiol. 2013;112:1958-61. [CrossRef] [PubMed] 

Reference as: Shekell T, Hypes C, Raz Y. Medical image of the week: ECG in PE. Southwest J Pulm Crit Care. 2015;10(1):44-6. doi: http://dx.doi.org/10.13175/swjpcc162-14 PDF

Medical Image of the Week: Idiopathic Pulmonary Artery Hypertension

Figure 1. EKG showing sinus rhythm, right bundle branch block and peaked ('pulmonary') p waves (arrow).

Figure 2. Two view chest X-ray showing right ventricular hypertrophy (arrows, note filling of the retrosternal space by an enlarged right ventricle in the lateral view) and enlarged central pulmonary arteries (arrowhead).

 

  Figure 3. Axial CT angiogram of the chest below the carina showing dilated pulmonary artery (diameter of pulmonary artery greater than aorta, arrow).

 

Figure 4. Panel A: Parasternal short axis view shows septal bowing to the left, a severely dilated right ventricle and a D-shaped left ventricle. Panel B: Four chamber view shows right atrial and ventricular dilatation.

A 39-year-old woman presented to the clinic with a history of progressive shortness of breath of 6-month duration associated with bilateral lower extremity edema, fatigue, lightheadedness, palpitations and occasional substernal chest pain. Her past medical history was unremarkable other than mild anemia. On physical exam her respiratory rate was 20 breaths per minute and O2 saturation 94% on room air by pulse oximetry. There was jugular venous distention at 12 cm, 2+ bilateral lower extremity edema, a 5/6 systolic murmur over the left sternal border with a sternal heave. Labwork was unremarkable except for an elevated BNP 657 (normal value < 100 pg/mL).

EKG (Figure 1) showed sinus rhythm with right bundle branch block. A 2-view chest X-ray (Figure 2) showed an enlarged right ventricle as well as dilated pulmonary arteries with no parenchymal infiltrates. CT angiography confirmed CXR findings (Figure 3) and was negative for pulmonary embolism. A 2D echocardiogram revealed a preserved left ventricle ejection fraction with right ventricular pressure of 80 mmHg + CVP, severe tricuspid regurgitation, decreased right ventricular function (as assessed by a Tricuspid annular plane systolic excursion of 10 mm) and flattened septum, suggestive of right ventricular overload (Figure 4). A right heart catheterization was performed revealing pulmonary pressures of 105/45 mmHg with a mean of 63 mmHg, a wedge pressure of 11 mmHg, a pulmonary vascular resistance of 13.19 Wood units and a cardiac output of 3.94 L/min.

The patient was admitted to the intensive care unit to start treatment with intravenous treprostinil and was eventually discharged home with subcutaneous treprostrinil.

Pulmonary arterial hypertension (PAH) is a disease of the pulmonary circulation characterized by a progressive elevation in pulmonary vascular resistance that leads to right ventricular failure and premature death. It is defined as a mean pulmonary artery pressure at rest of 25 mmHg or higher (1). Idiopathic (group 1) PAH requires the exclusion of parenchymal pathology or venous thromboembolic disease as well as a mean wedge pressure less than 15 mmHg. The initial symptoms of PH are the result of an inability to adequately increase cardiac output during exercise which eventually will progress to signs and symptoms of right ventricular failure such as lower extremity edema, syncope/presyncope and chest pain (2,3). Early recognition is of paramount importance to institute adequate treatment.

Roberto J. Bernardo, MD and Carlos Tafich Rios, MD

Internal Medicine Residency, Department of Medicine

University of Arizona, Tucson, AZ

References 

1. McLaughlin VV, Archer SL, Badesch DB, et al. ACCF/AHA 2009 expert consensus document on pulmonary hypertension: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association: developed in collaboration with the American College. Circulation. 2009. 119:2250-94. [CrossRef] [PubMed] 
2. Runo JR, Loyd JE. Primary pulmonary hypertension. Lancet. 2003. 361:1533-44. [CrossRef] [PubMed]
3. Peacock AJ. Primary pulmonary hypertension. Thorax. 1999;54:1107-18. [CrossRef] [PubMed]

Reference as: Bernardo RJ, Rios CT. Medical image of the week: idiopathic pulmonary artery hypertension. Southwest J Pulm Crit Care. 2014;9(2):101-3. doi: http://dx.doi.org/10.13175/swjpcc101-14   PDF

Medical Image of the Week: Malignant Pericardial Effusion and Cardiac Tamponade

Figure 1. EKG showing sinus tachycardia, low QRS voltage and electric alternans, suggesting pericardial effusion.

Figure 2. Chest X-ray pre- and post-pericardiocentesis. Panel A: Cardiomegaly with water bottle shape shown before procedure. Panel B: resolution after drainage of 1.8 L of pericardial fluid.

Figure 3. Echocardiogram showing massive pericardial effusion (dashed line), floating heart, and collapsed right atrium and ventricle that are consistent with cardiac tamponade.

Figure 4. Intra-pericardial space pressure tracing with maximum pressure measured at 25 mmHg.

A 53 year old woman with history of metastatic breast cancer presented to the emergency department (ED) with worsening shortness of breath for 2 weeks. She was initially diagnosed with grade III breast intraductal carcinoma was estrogen receptor, progesterone receptor, and HER2 negative 5 years earlier. A lumpectomy was performed followed by 4 cycles of chemotherapy with cyclophosphamide and taxol as well as radiation therapy. However, follow-up CT and MRI and subsequent biopsy demonstrated metastatic disease in the left adrenal gland, right ovary, and mediastinal lymph nodes, for which additional chemotherapy was started a month prior to presentation. In the ED, the patient was tachycardic and tachypneic. Vital signs showed BP 112/94 mmHg, HR 118 /min, RR 28 /min, temperature 97.5 °F, and SpO₂ 97 % with room air. EKG showed sinus tachycardia, low QRS voltage with electric alternans (Figure 1), and chest x-ray demonstrated cardiomegaly with a water bottle shaped heart (Figure 2A), suggesting pericardial effusion. Over the hour at ED, patient developed sudden hypotension with BP of 78/44. 1 L of normal saline was administrated immediately, and patient was transferred to cardiac catherization laboratory for emergent pericardiocentesis. Echocardiogram before the procedure demonstrated massive pericardial effusion and a floating heart in the pericardial space (Figure 3). Intra-pericardial pressure was measured at 25 mmHg (Figure 4). A total of 1.8 L of sanguineous fluid was drained. Pericardial fluid cell count with differential and chemistry showed WBC 2444 /μL, RBC 1480000 /μL, lymphocytes 32 /μL , neutrophils 64 /μL, glucose 108 mg/dL, and protein 5.2 g/dL, and cytology analysis with fluid demonstrated adenocarcinoma, confirming the diagnosis of malignant pericardial effusion and cardiac tamponade. Chest x-ray after the procedure showing resolution of the water bottle-shaped heart (Figure 2B). Elective thoracotomy with pericardiectomy was performed the next day, and patient was eventually discharged in stable condition.

Pericardial effusion seen in cancer patients may results from several sources. Constrictive pericarditis with pericardial effusion can arise as a complication of radiation therapy. Uremia and certain medications can induce pericardial effusion as well. Metastatic cardiac involvement may causes pericardial effusion. A previous autopsy study showed 10.7 % of patients with underlying malignancy had metastatic disease in the heart (1). Adenocarcinoma is the most frequently found cell type, and lung cancer, malignant lymphoma and breast cancers are the most common primary tumors metastasizing to the heart. Symptoms of malignant pericardial effusion include shortness of breath, cough, chest pain, and edema. Vaitkus et al. (2) proposed three goals in the management of symptomatic malignant pericardial effusion:1) relief of immediate symptoms, 2) determination of cause, and 3) prevention of recurrence (2). No single modality has been proved to be superior since most patients with malignant pericardial effusion need more than one therapeutic modality. Pericardiocentesis is commonly used for acute symptomatic relief while other chemical or mechanical modalities such as systemic chemotherapy, radiation therapy, intrapericardial sclerosing agents, indwelling pericardial catheter, or thoracotomy with pericardiectomy are options to prevent relapse.

Seongseok Yun, MD PhD; Juhyung Sun, BS; Rorak Hooten, MD; Yasir Khan, MD;Craig Jenkins, MD

Department of Medicine, University of Arizona, Tucson, AZ 85724, USA

References

1. Klatt EC, Heitz DR. Cardiac metastases. Cancer. 1990;65(6):1456-9. [CrossRef]
2. Vaitkus PT, Herrmann HC, LeWinter MM. Treatment of malignant pericardial effusion. JAMA. 1994;272(1):59-64. [CrossRef] [PubMed] 

Reference as: Yun S, Sun J, Hooten R, Khan Y, Jenkins C. Medical image of the week: malignant pericardial effusion and cardiac tamponade. Southwest J Pulm Crit Care. 2014;8(6):343-6. doi: http://dx.doi.org/10.13175/swjpcc048-14 PDF