Hemodynamic Findings of Effusive-Constrictive Pericarditis
- Anand D. Shah, MD
- Daniel L. Molloy, MD
- John E.A. Blair, MD
- Daniel L. Molloy, MD
A 64-year-old man with rheumatoid arthritis presented with progressive abdominal and leg swelling, anorexia, and dyspnea for several years. Physical examination was notable for a pericardial knock, pulsatile hepatomegaly, and lower extremity edema. The jugular vein was distended past the angle of the jaw and did not decrease with inspiration (Kussmaul sign). Transthoracic echocardiography demonstrated normal left ventricular function, a thickened pericardium, and a large pericardial effusion. Computed tomography showed the pericardium to measure 8 mm (normal, <3 mm). To clarify a diagnosis of symptomatic pericardial effusion versus constrictive pericarditis, the patient was referred for left-side and right-side heart catheterization and pericardiocentesis.
Left and right ventricular pressures were transduced simultaneously with right atrial pressure (RAP) at baseline; interventricular dependence of left and right ventricular filling was noted ( Fig. 5.1 A, arrowheads , scales optimized), along with a dip-and-plateau pattern of ventricular filling. RAP was severely elevated and failed to decrease with inspiration ( Fig. 5.1 B, asterisk ). The preserved y descent in RAP was not consistent with tamponade. Intrapericardial pressure was measured with RAP at baseline ( Fig. 5.1 C) and after complete drainage of pericardial fluid ( Fig. 5.1 D). RAP was dissociated from intrapericardial pressure, remaining elevated at 25 mm Hg, despite normalization of intrapericardial pressure to 0 mm Hg. The typical, exaggerated y descent of pericardial constriction was more apparent after pericardiocentesis because the holodiastolic four-chamber impediment to filling associated with tamponade was eliminated, leaving only the limitation to filling in mid- and end-diastole, characteristic of constrictive pericarditis. Thus the findings demonstrated that the patient’s elevated filling pressures were related to constrictive pericarditis. Despite adjustment of the patient’s immunosuppressive regimen, severe congestive symptoms persisted. The patient underwent successful pericardiectomy, at which time the diagnosis was confirmed. Pericardial involvement is noted in 50% of patients with rheumatoid arthritis, although ≥90% are asymptomatic.
Reference
1. Prasad M, Hermann J, Gabriel SE, et. al.: Cardiorheumatology: cardiac involvement in systemic rheumatic disease.Nat Rev Cardiol 2015; 12: pp. 168-176.
Hypoxemia Due to Patent Foramen Ovale in the Setting of New Right Hemidiaphragmatic Paralysis
- Cory R. Trankle, MD
- Hem L. Bhardwaj, MD
- Walter H.J. Paulsen, MD
- John D. Grizzard, MD
- Rachit D. Shah, MD
- Zachary M. Gertz, MD, MBE
- Hem L. Bhardwaj, MD
A 58-year old man with no history of cardiac pathology presented with dyspnea and was found to be hypoxemic (oxygen saturation, 88% on room air) with platypnea-orthodeoxia. The symptoms had started soon after a laparoscopic cholecystectomy 3 weeks before.
Imaging revealed new right hemidiaphragmatic paralysis (confirmed with sniff testing showing paradoxic motion) and no pulmonary embolism ( Fig. 5.2 A–B). Transthoracic echocardiography with agitated saline demonstrated the early appearance of a large number of microbubbles in the left side of the heart, consistent with a right-to-left interatrial shunt ( Fig. 5.2 C, Online 
). Transesophageal echocardiography confirmed a patent foramen ovale (PFO) with near continuous right-to-left flow ( Fig. 5.2 D–E).
). (D and E) Interatrial septum by transesophageal echocardiography revealing PFO with right-to-left flow. (F) Intracardiac echocardiography showing deployment of Amplatzer Septal Occluder (St. Jude Medical, St. Paul, Minnesota). (G) Chest CT after diaphragmatic plication showing improvement in hemidiaphragm elevation and decreased right atrial compression. (H) Postprocedural bubble study revealing resolution of shunt, including during provocative maneuvers (Online 
and ). LA , left atrium; LV, left ventricle; PFO , patent foramen ovale; RA , right atrium; RV , right ventricle.
The patient was referred for percutaneous PFO closure. Pulmonary vein oxygen saturation was 96% (arterial room air saturation, 87%). A 25-mm Amplatzer cribriform Septal Occluder device (St. Jude Medical, St. Paul, Minnesota) was deployed, and the patient’s arterial saturation immediately improved to 96% ( Fig. 5.2 F). His symptomatic shortness of breath was improved but not completely resolved, so he was referred for diaphragmatic plication. After successful plication, the patient’s dyspnea nearly completely resolved ( Fig. 5.2 F–H, Online 
and ).
Platypnea-orthodeoxia syndrome is a rare phenomenon that can be caused by a hemodynamically significant PFO. It has been reported several times as a complication after right pneumonectomy , and less frequently as a result of right hemidiaphragmatic elevation. , Timely diagnosis and closure of the PFO can lead to rapid correction of hypoxemia.
References
1. Kaufman DA, Ravi S, Dadu R, Horowitz D, Logue MA: Severe hypoxemia and orthodeoxia following right pneumonectomy.Am J Respir Crit Care Med 2011; 184: pp. e1-e2.
2. Bhattacharya K, Birla R, Northridge D, Zamvar V: Platypnea-orthodeoxia syndrome: a rare complication after right pneumonectomy.Ann Thorac Surg 2009; 88: pp. 2018-2019.
3. Maholic R, Lasorda D: Successful percutaneous closure of a patent foramen ovale causing hypoxia in the setting of an elevated hemidiaphragm due to Guillain-Barré syndrome.J Invasive Cardiol 2006; 18: pp. 434-435.
4. Sakagianni K, Evrenoglou D, Mytas D, Vavuranakis M: Platypnea-orthodeoxia syndrome related to right hemidiaphragmatic elevation and a “stretched” patent foramen ovale.BMJ Case Rep 2012; 2012: bcr-2012-007735
Aortoarteritis With Chronic Total Occlusion of All Neck Vessels: Percutaneous Stenting to Salvage Intractable Syncope
- Nagaraja Moorthy, DM
- Rangaraj Ramalingam, DM
- Subramanyam K. Setty, DM
- Shivanand S. Patil, DM
- Manjunath C. Nanjappa, DM
- Rangaraj Ramalingam, DM
A 42-year-old woman was admitted with a history of recurrent syncope of more than 10 to 15 episodes per day for more than 3 months that worsened over 1 month. She was diagnosed with aortoarteritis type I 3 years before an angiography showed total occlusion of bilateral subclavian ( Fig. 5.3 A–B, Online 
A–B), bilateral vertebral, and left common carotid arteries ( Fig. 5.3 C, Online 
C). The right common carotid artery had diffuse 70% lesion. Her coronary arteries, renal arteries, and aorta were normal. Because she was asymptomatic and considering the discouraging results of percutaneous interventions in aortoarteritis, she was advised medical follow-up and treated with immunosuppression. Just before additional computed tomography (CT) angiography of neck vessels, she had acute left faciobrachial monoparesis. All four neck vessels were occluded ( Fig. 5.3 D–E) and the sole brain was supplied by tiny collaterals. CT of the brain showed right frontotemporoparietal acute infarct ( Fig. 5.3 F). In view of the urgency of revascularization and risks involved in surgery, it was decided to perform urgent percutaneous angioplasty. Because the right common carotid artery was the latest to block, it was decided to open it because the success rate could be better when compared with the other three neck vessels. The right carotid artery was hooked with 6F shuttle sheath. The lesion was crossed with a 0.014-inch Pilot 150 wire (Abbott Vascular, Santa Clara, California) ( Fig. 5.4 A, Online 
A). However, because there was no support over this wire, it was exchanged to a 0.035-inch exchange wire (Medtronic, Inc., Minneapolis, Minnesota) to place at the distal end of the wire in the external carotid artery ( Fig. 5.4 B, Online 
B). In view of the patient’s recent stroke and to prevent embolism, hardware manipulation was minimized and it was decided to perform direct stenting without predilation. A 6 mm × 100 mm Complete SE self-expanding stent (Medtronic, Inc.) distal edge was meticulously placed just at the bifurcation of the common carotid artery and deployed. Poststenting underexpansion of the stent was noted ( Fig. 5.4 C, Online 
C). Postdilation was done using a 7 mm × 20 mm NuMed (B. Braun Medical Inc., Hopkinton, New York) balloon catheter. The final result showed a well-expanded stent with significantly improved perfusion to the brain ( Fig. 5.4 D, Online 
D). No procedure-related complications were noted and the patient had complete relief from syncope. The carotid Doppler at 6 months follow-up showed the patent stent ( Fig. 5.4 E, Online 
E) and she remained asymptomatic.
A). (B) Left common carotid artery angiography showing chronic total occlusion with bridging collaterals (Online 
B). (C) Left subclavian artery angiography showing chronic total occlusion of left subclavian and left vertebral artery (Online 
C). (D) Computed tomography (CT) angiography of neck vessels showing total occlusion of all four neck vessels. (E) CT angiography volume-rendered imaging of neck vessels showing total occlusion of all four neck vessels. (F) CT of brain showing right frontotemporoparietal infarct.
A). (B) The right common carotid artery lesion was crossed using a 0.35-inch exchange length wire (Online 
B). (C) Poststenting of the right common carotid artery using Complete SE stent (Medtronic, Minneapolis, Minnesota) showing an underexpanded stent (Online 
C). FIG. 5.4 , cont’d (D) Poststenting right common carotid angiography showing fully expanded stent with improved brain perfusion (Online 
D). (E) Right common carotid Doppler at 6 months follow-up showing patent stent (Online 
E).
Chronic total occlusions of neck vessels are not uncommon in aortoarteritis. Chronic total occlusions of all neck vessels presenting as recurrent syncope are very rare. Although percutaneous stenting of atherosclerotic total occlusion of the carotid artery is considered as contraindication, in rare conditions, such as aortoarteritis, percutaneous stenting could be considered as a safe and effective alternative to surgery.
Intraluminal Fibrous Webs in Brachial Artery Fibromuscular Dysplasia
- Yoshito Kadoya, MD
- Kan Zen, MD, PhD
- Satoaki Matoba, MD, PhD
- Kan Zen, MD, PhD
An 80-year-old woman diagnosed as having severe aortic stenosis underwent preoperative coronary angiography through the left radial artery for transcatheter aortic valve implantation. A 0.025-inch guidewire was advanced into the left brachial artery for sheath insertion. Upper extremity angiography was performed because it was difficult to pass the wire through the artery; the angiogram showed alternating stenoses and dilatations (i.e., a “string of beads” appearance) in the left brachial artery ( Fig. 5.5 A). The optical coherence tomography scan showed thickening of the middle layer ( Fig. 5.5 B, Online 
), causing intraluminal protrusion of the arterial segment ( Fig. 5.5 C). Angioscopy demonstrated intraluminal fibrous webs (arrows) as white, wall-like structures protruding into the lumen and contacting the wire (arrowheads); no thrombus was observed ( Fig. 5.5 D–E, Online 
). Therefore the diagnosis was brachial artery fibromuscular dysplasia (FMD). Because the patient was asymptomatic and no pressure gradient was observed across the FMD segment, no intervention or additional medical treatment was performed. Subsequently, the sheath was successfully passed through the narrowing segment, and transradial coronary angiography was completed. Further investigation showed no FMD lesions in other arterial territories.
), causing (C) intraluminal protrusion of the arterial segment ( arrows ). (D and E) Angioscopy showing intraluminal fibrous webs ( arrows ) as white, wall-like structures protruding into the lumen and contacting the wire ( arrowheads ). No thrombus is observed (See Online 
).FMD is a nonatherosclerotic, noninflammatory angiopathy that causes narrowing of medium-sized arteries, and it is characterized by fibrodysplastic changes. Although catheter-based angiography is the gold standard for diagnosing FMD, it may be inadequate for visualizing intraluminal fibrous webs, whereas optical coherence tomography and angioscopic imaging can clearly show the presence of webs in the brachial artery. In the era of transradial catheter intervention, the importance of diagnosing brachial artery FMD should be recognized.
Reference
1. Olin JW, Gornik HL, Bacharach JM, et. al.: Fibro-muscular dysplasia: state of the science and critical unanswered questions: a scientific statement from the American Heart Association.Circulation 2014; 129: pp. 1048-1078.
A Rare Radial Artery Anatomic Variant: Look for the Pulse on the Dorsum of the Wrist!
- Arjun Venkatesh, BSc
- Erin Wagner, RT(R)
- Jodi Klebe, RN
- Jessica Schmidt, CVT/RCIS
- Laila Payvandi, MD
- Wassef Karrowni, MD
- Erin Wagner, RT(R)
Several radial artery anatomic variations have been described. , These are especially important for the radiologists in the catheterization laboratory for troubleshooting, especially with the growing popularity of the radial artery as the preferred access site for diagnostic and interventional coronary angiographic procedures. Variation in the origin of the radial artery is a common anomaly in the upper limb. However, the distal part of its course shows a constant pattern. Here we report the unusual course of a duplicate radial artery in the lateral forearm and the dorsum of the hand.
A 56-year-old woman presented to our clinic reporting exertional chest pain. A nuclear stress test was suggestive of ischemia in the inferior wall. This was followed by cardiac catheterization, which was planned from the right radial approach. The patient had 1+ right radial pulse with normal results on Allen test. Access was obtained in the right radial artery using the Seldinger approach. A 6F Slender sheath (Terumo, Tokyo, Japan) was placed, and intraarterial nitroglycerin was infused. Advancing a Tiger catheter (Terumo) over a 0.035-inch J wire was challenging because as the wire could not be advanced past the midforearm level. Contrast injection was performed through the sheath and demonstrated a small radial artery with another larger anomalous vessel originating at the elbow level and migrating laterally ( Fig. 5.6 ). A 2+ pulse was palpated at the dorsum of the hand. Another 6F Slender sheath was placed under ultrasound guidance in the duplicate vessel, and coronary angiography was completed with no difficulty ( Fig. 5.7 ).
