A Focus on Cardiology
Giant Hiatal Hernia Mimicking Cardiac Tamponade
Ranjit Nair, MD, and Yehia Y. Mishriki, MD, FACP
Allentown, PA
A 67-year-old female presented to the emergency room with multiple episodes of syncope. The initial work-up included an EKG, which showed a complete heart block. The patient went on to receive a permanent pacemaker and tolerated the procedure well.
Two hours after the procedure, she developed shortness of breath, dizziness, and a drop in her blood pressure. She denied chest pain or palpitations. Her physical exam revealed distant heart sounds with positive jugular venous pulsations.
Figure 1. A 4-chamber view of the heart showing echo lucent space posterior to the left atrium. TTE showing echo lucent space (E) compressing the left atrium. RA: right atrium, LA: left atrium, RV: right ventricle, LV: left ventricle
Vital signs at that time showed hypotension with blood pressure at 68/42 mmHg, tachycardia of 110 beats per min, and pulse oximetry showing 88% on a 2 L nasal cannula. An immediate EKG showed sinus tachycardia. Anticipating complications of the pacemaker procedure, an emergent bedside echocardiogram was done, which showed a large echo-free space adjacent to the left atrium with marked compression (Figures 1-3).
Figure 2. Parasternal view (long axis) of the heart. TTE showing echo lucent space (E) compressing the left atrium. RA: right atrium, LA: left atrium, RV: right ventricle, LV: left ventricle
Figure 3. Parasternal view (short axis) of the heart. TTE showing echo lucent space (E) compressing the left atrium.
Chest x-ray showed large intrathoracic hiatal hernia in the mediastinum (Figure 4). The patient was placed NPO and nasogastric decompression was done with a nasogastric tube. Her symptoms and blood pressure improved.
Figure 4. Chest x-ray showing intrathoracic hiatal hernia compressing the heart.
The left atrium is an inferoposteriorly-located cardiac chamber with a low pressure cavity and a thin wall, making it vulnerable to impression from any adjacent structures. Compression of the left atrium by extra-cardiac structures—hiatal hernia being the most common—is a rare cause of dyspnea and hemodynamic instability, which would mimic symptoms of pericardial tamponade. This could be easily visualized by transthoracic echocardiography (TTE) or with a chest x-ray.■
References
1.van Rooijen JM, van den Merkhof LFM. Left atrial impression: a sign of extra-cardiac pathology. Eur J Echocardiogr. 2008;9:661-664.
2.Moore J, Fraser J. Outside the box: extra-pericardial tamponade due to acute recurrence of hiatus hernia. Ann Thorac Surg. 2010;89:1654-1656.
Intrahepatic Artery Aneurysms
Vera Rivera, MD, and Scott Carlos, MD
Wisconsin Rapids, WI and Wheeling, WV
A 68-year-old female was admitted for abdominal pain and elevated WBC at the emergency room. Upon arrival to the ward, a rapid response was called on the patient. She was complaining of severe abdominal pain and was hypotensive and diaphoretic. Examination of the abdomen revealed no distention, hypoactive bowel sounds, severe direct and rebound tenderness, as well as involuntary guarding.
IVF bolus was initiated to stabilize the blood pressure and patient was brought immediately to radiology. A CT scan of the abdomen and pelvis showed large amount of hemoperitoneum with bleeding appearing to be originating from a 1.7 cm pseudoaneurysm in the postero-medial aspect of the right lobe of the liver (Figure 1). In addition, the scan showed three small pseudoaneurysms within the right hepatic lobe.
The patient was intubated and underwent visceral angiography, which revealed multiple intrahepatic arterial aneurysms with active extravasation from the right lobe. She subsequently underwent embolization of the right hepatic artery with gelfoam and coils (Figure 2), and paracentesis of 1,200 cc of blood. The patient had a complicated course in the cardiovascular ICU but was discharged with improving clinical status on the 23rd hospital day.
Hepatic artery aneurysm (HAA) are extremely rare and most diagnosis are often made incidentally or postmortem. They account for 20% of visceral artery aneurysms.1 It is twice as common in men, and majority of patients are asymptomatic prior to rupture of the HAA. When they do become symptomatic, about 55% have abdominal pain and less than half of cases have GI bleeding. Physical exam is usually unremarkable unless there is a large pulsatile mass and the patient’s body habitus allows palpation. Consequently, shock may also be the presenting picture after HAA rupture (as with our patient) which occurs in approximately 10% of cases.2
Therapeutic approaches vary. Transcatheter arterial ablation is becoming an increasingly popular alternative, and was performed on our patient.3 ■
References:
1.Luebke T, Heckenkamp J, Gawenda M, et al. Combined endovascular-open surgical procedure in a great hepatic artery aneurysm. Ann Vasc Surg. 2007;21(6):807-812.
2.O’Driscoll D, Oliff SP, Oliff JF. Hepatic artery aneurysm. Br J Radiol. 1999;72(862):1018-1025.
3.Dwivedi AJ, Greben C, Krishnasastry KV. Catheter embolization of a hepatic artery aneurysm, a case report. Vasc Endovasc Surg. 2006;40:79-83.
Digit-like Left Atrial Myxoma
Jorge A Brenes Salazar, MD, and Hemal Kadakia, MD
Minnesota, MN
A 45-year-old male presented to the emergency department with an episode of exertional syncope. He had not suffered from loss of consciousness prior to that visit. He sustained no injuries. He had no prodromal symptoms, and denied any residual confusion, abnormal movements, tongue biting, or incontinence after quickly recovering consciousness.
His past medical history was significant for hypertension and tobacco dependence. His only medication was hydrochlorothiazide 25 mg daily. His vital signs were within normal limits and orthostatic maneuvers were negative. Physical examination was remarkable for an intermittent diastolic murmur best hear at the apex. His resting ECG showed normal sinus rhythm and chest x-ray; CBC and electrolytes were within normal limits.
He underwent a thransthoracic echocardiogram, which showed a digit-like highly mobile mass in the left atrium—which was further characterized by transesophageal echocardiogram. The patient was admitted, started on anticoagulation, and underwent surgical resection of the mass, which showed a striking macroscopic resemblance to the echocardiographic images and proved to be an atrial myxoma by histologic examination. The patient did well after surgery and had no recurrence of his index symptoms.
Atrial myxomas are the most common primary cardiac tumors, representing about 50% of these. Three of every 4 are found in the left atrium, but they can be present in other chambers. Females are affected in 65% of sporadic myxomas cases.1 There may be a familial predisposition for these types of tumors in as many as 10% of the cases; inheritance follows an autosomal dominant pattern.
Macroscopically, myxomas are gelatinous with a white, yellow, or black color, and a polypoid or round appearance. Many times they are discovered incidentally, but they can manifest with non-specific symptoms of fever, arthralgias, weight loss, right- or left-sided heart failure, or life-threatening complications such as embolic myocardial infarction, stoke, or sudden cardiac death.2 Polypoid myxomas have a higher tendency to cause embolic events as compared to round myxomas.3 Because of their highly vascularized nature, they can feed directly from epicardial coronary arteries, and this can incidentally be seen during a coronary angiogram.
Large atrial myxomas that are highly mobile can protrude into the atrioventricular valves during diastole and impair ventricular filling, resulting in decreased cardiac output and syncope.4 On physical examination, the most typical findings of large left atrial myxomas include a loud S1 due to prolonged opening of the mitral valve, a murmur similar to mitral stenosis when there is obstruction or suggestive of mitral regurgitation when there is invasion of the leaflets, and a classic early diastolic sound called a tumor plop.
The imaging gold standard for diagnosis continues to be transthoracic echocardiography, although transesophageal echocardiography has increased sensitivity and provides more accurate definition of the anatomical features of the tumor with respect to the cardiac structures. Cardiac MRI and CT have been increasingly used to define anatomical features of myxomas and help differentiate these from intracardiac thrombi.5 Surgical resection is the standard of care, since embolic complications and the tendency for intracavitary thrombus formation are not rare.6 ■
References:
1.Stevens LM, Lapierre H, Pellerin M, et al. Atrial versus biatrial approaches to cardiac myxomas. Interact Cardiovasc Thorac Surg. 2003;2(4):521-525.
2.Marta L, Peres M, Alves M, Ferreira da Silva G. Giant left atrial myxoma presenting as acute myocardial infarction. Rev Port Cardiol. 2012;31(12):815-819
3.Ha JW, Kang WC, Chung N. Echocardiographic and morphologic characteristics of left atrial myxoma and their relation to systemic embolism. Am J Cardiol. 1999;83:1579-1582.
4.Strecker T, Agaimy A. Giant left atrial myxoma causing drop attacks by prolapsing into the mitral valve. Int J Clin Exp Pathol. 2012;5(9):996-909.
5.Scheffel H, Baumueller S, Stolzmann P, et al. Atrial myxomas and thrombi: comparison of imaging features on CT. AJR Am J Roentgenol. Mar 2009;192(3):639-645.
6.Pinede L, Duhaut P, Loire R. Clinical presentation of atrial myxoma: a series of 112 consecutive cases. Medicine. 2001;80(3):159-172.
Cocaine-Induced QTc Prolongation
Mrugesh Patel, MD, Umang Shah, MBBS, MPH, CPH, and Charles Richard Conti, MD, MACC, Dr HC, FCP(SA), FESC, FAHA
Orlando, FL
A 48-year-old Caucasian female presented with chest pain over the past few days. She had a syncopal episode for few seconds, followed by consciousness without any associated confusion. She admitted smoking crack cocaine 2 days prior to the onset of her symptoms. She denied any other symptoms or taking any medications at home. The vital signs and physical exam were normal, as were basic chemistry and hematology. Troponin T was < 0.03 on 3 occasions 8 hours apart. Chest x-ray and CT of head were unremarkable. Twelve lead ECG showed prolonged QTc interval of 634 ms with T wave inversions (Figure 1). Serial ECGs showed decrease in her QTc interval to 483 ms before discharge (Figure 2). The coronary angiography showed mild non-obstructive coronary artery disease. Six months prior to admission, her ECG showed QTc interval of 445 ms with normal T waves (Figure 3).
Cocaine use is very common in US patient population and is a frequent cause of chest pain admissions in the hospitals across the country. Most of the time physicians are concerned about cocaine-induced coronary ischemia and myocardial infarction. However, other potential cardiovascular complications can also arise from cocaine use, and can lead to significant morbidity and mortality.
Cocaine has robust effect on the myocardial conducting system leading to electrical abnormalities, such as the ones observed in our patient. The literature contains evidence to suggest that cocaine causes QTc prolongation.1,2 While the exact mechanism has not been established, there is some evidence to say that cocaine-induced sodium and potassium channel blockade may be responsible for this effect.3 Cocaine also leads to numerous other types of arrhythmias, such as Brugada syndrome, bundle-branch block, ventricular fibrillation, ventricular tachycardia and accelerated idioventricular rhythm, heart block, torsades de pointes, and a variety of supraventricular tachycardias.4
Our patient had dynamic systolic dysfunction evident on two separate echocardiograms 4 months apart. Cocaine has also been shown to cause cardiomyopathy and myocarditis. Various mechanisms are responsible for these changes—such as myocardial ischemia, direct toxic effect of cocaine causing myocardial necrosis, tachycardia-induced cardiomyopathy, and autoimmune reaction to cocaine and levamisole (used as a cutting agent with cocaine).5 ■
References:
1.Magnano AR, Talathoti NB, Hallur R, et al. Effect of acute cocaine administration on the QTc interval of habitual users. Am J Cardiol. 2006;97(8):1244-1246.
2.Haigney MC, Alam S, Tebo S, et al. Intravenous cocaine and QT variability. J Cardiovasc Electrophysiol. 2006;17(6):610-616.
3.Wood DM, Dargan PI, Hoffman RS. Management of cocaine-induced cardiac arrhythmias due to cardiac ion channel dysfunction. Clin Toxicol (Phila). 2009 Jan;47(1):14-23.
4.Om A, Ellenbogen KA, Vetrovec GW. Cocaine-induced bradyarrhythmias. Am Heart J. 1992; 124(1):232-234.
5.Bertolet BD, Freund G, Martin CA, et al. Unrecognized left ventricular dysfunction in an apparently healthy cocaine abuse population. Clin Cardiol. 1990;13(5):323-328.