75. Case Report: Coronary Vasospasm Presenting as STEMI – UCSF

CardioNerds (Amit Goyal & Daniel Ambinder) join UCSF cardiology fellows (Emily Cedarbaum, Matt Durstenfeld, and Ben Kelemen) for some fun in San Francisco! They discuss a informative case of ST-segment elevation (STEMI) due to coronary vasospasm. Dr. Binh An Phan provides the E-CPR and program director Dr. Atif Qasim provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai.

Jump to: Patient summaryCase mediaCase teachingReferences

CardioNerds (Amit Goyal & Daniel Ambinder) join UCSF cardiology fellows (Emily Cedarbaum, Matt Durstenfeld, and Ben Kelemen) for some fun in San Francisco! They discuss a fascinating case of ST-segment elevation (STEMI) due to coronary vasospasm. Dr. Binh An Phan provides the E-CPR and program director Dr. Atif Qasim provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Subscribe to our newsletter- The Heartbeat
Support our educational mission by becoming a Patron!
Cardiology Programs Twitter Group created by Dr. Nosheen Reza

Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

Patient Summary

A man in his mid-50s with alcohol use disorder, cirrhosis, atrial fibrillation, and alpha thalassemia complicated by iron overload presented with hematemesis. He was tachycardic and hypotensive. Labs were notable for Hgb 8.1 (baseline of 10.2), INR 1.3, lactate 4.2, and ferritin 4660. He was started on IV PPI and octreotide. Course was complicated initially by Afib with RVR with hypotension. Subsequently, the patient developed unstable VT requiring CPR. Post-code EKG showed inferolateral ST elevations. Troponin-I rose from 19 to 225 and his pressor requirement continued to increase despite resolution of his GIB. TTE showed LVEF 42% with new inferolateral wall motion abnormalities, normal RV systolic function, severe mitral regurgitation, and small pericardial effusion. After treatment of his GIB by IR and GI, he underwent an urgent LHC which showed 30% stenosis in proximal LAD, 70% in LADD2, and 95% in distal RCA. Coronary spasm was noted in all vessels. Intracoronary nitroglycerin and nicardipine were administered with significant improvement in spasm and resolution of STE on EKG. Vasopressors were quickly weaned off after. He was eventually stabilized, extubated, and started on an oral nitrate and calcium channel blocker. Repeat TTE showed normalized systolic function without any wall motion abnormalities.  


Case Media

A. Baseline ECG – atrial fibrillation
B. ECG with inferior STEMI

CORS – left system
CORS- RCA pre-vasodilator
CORS- RCA post-vasodilator

Episode Schematics & Teaching

Coming soon!


The CardioNerds 5! – 5 major takeaways from the #CNCR case

  1. What are the cardiac manifestations of hemochromatosis? 
    • Cardiac hemochromatosis encompasses cardiac dysfunction from either primary or secondary hemochromatosis. Initially, hemochromatosis leads to diastolic dysfunction and arrhythmias. In later stages, it can lead to dilated cardiomyopathy.  
    • Diagnosis of iron overload is established by elevated transferrin saturation (>55%) and elevated serum ferritin (>300 ng/mL). Genetic testing for mutations in the HFE gene should be pursued. 
    • Cardiac MRI with measurement of T2* relaxation times is the diagnostic test of choice as it can both detect and quantify myocardial iron overload. The iron content in the myocardial tissue is inversely proportional to the time constant of decay for relaxation time. Thus the higher the iron content, the shorter T2* relaxation time.  
  2. What are the causes of ST-segment elevation on EKG besides acute plaque rupture or vasospasm? 
    • Pericarditis: in acute pericarditis, ST elevation can be seen diffusely in all leads, with PR segment depression (except lead aVR +/- V1). The diffuse ST elevations are due to involvement of subepicardial layer of the ventricular wall. The PR depressions are due to involvement of the subepicardial layer of the atrial wall.  
    • Stress CM: The ECG findings of stress cardiomyopathy may be indistinguishable from STEMI secondary to acute plaque rupture. 
    • Brugada syndrome: >2 mm ST-segment elevation in the right precordial leads followed be a negative T wave can be seen in patients with Type 1 Brugada. Type 2 and Type 3 Brugada will have STE as well but with different morphologic criteria.  
    • Electrolyte abnormalities: hyperkalemia can sometimes cause ST elevation. Other EKG findings of hyperkalemia include widened QRS, tall and peaked T waves, low-amplitude or lack of P waves, high grade AV Block, sine wave, and/or ventricular fibrillation or PEA. 
    • Pulmonary embolism: the classic EKG features of PE are S1Q3T3 with signs of RV strain (RBBB, RAD) though these are neither sensitive or specific. Sometimes, ST elevation in aVR and right-sided precordial are seen in massive PE due to RV overload, dilation, and/or ischemia (see the Cedars-Sinai episode for more details!).  
    • Cardioversion: striking ST-segment elevation, often >10mm, can be seen after cardioversion but only lasts 1-2 minutes.  
    • Raised ICP: can mimic acute myocardial infarction with widespread T-wave inversions +/- STE (or depression). Other non-cardiac causes, albeit rare causes, include significant gastrointestinal visceral distension, pneumonia, and pancreatitis.  
  3. What are the two types of ischemic mitral regurgitation (IMR)? 
    • IMR is often a complication of ischemic heart disease and is associated with a worse prognosis across a variety of settings. Ischemic MR can occur due to a primary cause (e.g., abnormality of the valve apparatus and specifically papillary muscle rupture) or secondary cause (e.g., acutely from ischemia and chronically from a complex pathophysiologic changes).  
    • In chronic IMR, regional and/or global LV systolic dysfunction and ventricular remodeling can cause restricted leaflet motion. There can be outward papillary muscle displacement and when this happens, mitral leaflet coaptation moves apically away from the mitral annulus. Further, scarring of the papillary muscles may produce further mitral leaflet tethering and LV dilation can lead to mitral annular dilation. The posterior mitral annulus may contract less as well (which contributes to as much as 25% of the closure of the mitral orifice during systole). The ultimate results is poor leaflet coaptation and mitral regurgitation.  
    • MR secondary to papillary muscle rupture after an acute MI will almost certainly require surgery; while secondary MR from acute ischemia will often respond to revascularization. The treatment of chronic ischemic MR is a topic for another Cardionerds Episode so stay tuned!  
  4. What’s the pathogenesis of coronary vasospasm? 
    • In coronary vasospasm, the coronary arteries – and specifically the vascular smooth muscle layer – constricts due to various causes including emotional distress, changes in sympathetic tone, cocaine, or cigarette smoking, leading to myocardial ischemia.  
    • The causes and mechanisms of coronary vasospasms are still poorly understood but there are a few potential mechanisms proposed. 
      • Autonomic nervous system: increase in sympathetic tone can induce coronary vasospasms. Vasospasms more commonly occur at night during rapid eye movement sleep, when a reduction in vagal activity is associated with an increase in adrenergic activity.  
      • Inflammation: chronic inflammation and cigarette smoking are shown to be associated with vasospasm. Patients with vasospasm are found to have elevated hs-CRP, IL-6, and peripheral WBC.  
      • Other mechanisms have also been proposed including smooth muscle cell hypercontractility, oxidative stress, and genetics 
  5. What’s the treatment for coronary vasospasm? 
    1. Any factor that may precipitate coronary vasospasm, especially smoking, should be avoided. There are additionally certain medications that should be avoided including non-selective beta blockers like propranolol and triptans.  
    2. For medical treatment, long-acting calcium channel blockers can be used, especially taken at nighttime when attacks of coronary vasospasm are frequent 
    3. Long-acting nitrates can also be added to prevent recurrent attacks if calcium channel blockers alone are inadequate 

References

  1. Gulati, V., Harikrishnan, P., Palaniswamy, C., Aronow, W. S., Jain, D., & Frishman, W. H. (2014). Cardiac involvement in hemochromatosis. Cardiology in review22(2), 56–68. 
  2. Wang, K., Asinger, R. W., & Marriott, H. J. (2003). ST-segment elevation in conditions other than acute myocardial infarction. The New England journal of medicine349(22), 2128–2135.  
  3. Báez-Ferrer, N., Izquierdo-Gómez, M. M., Marí-López, B., Montoto-López, J., Duque-Gómez, A., García-Niebla, J., Miranda-Bacallado, J., de la Rosa Hernández, A., Laynez-Cerdeña, I., & Lacalzada-Almeida, J. (2018). Clinical manifestations, diagnosis, and treatment of ischemic mitral regurgitation: a review. Journal of thoracic disease10(12), 6969–6986.  
  4. Hung, M. J., Hu, P., & Hung, M. Y. (2014). Coronary artery spasm: review and update. International journal of medical sciences11(11), 1161–1171.  
  5. Slavich, M., & Patel, R. S. (2016). Coronary artery spasm: Current knowledge and residual uncertainties. International journal of cardiology. Heart & vasculature10, 47–53.  

CardioNerds Case Reports: Recruitment Edition Series Production Team

71. Case Report: Post-MI Ventricular Septal Rupture – University of Michigan

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Michigan cardiology fellows (Apu Chakrabarti, Jessica Guidi, and Amrish Deshmukh) for some craft brews in Ann Arbor! They discuss a challenging case of Ventricular Septal Rupture after acute MI. Dr. Kim Eagle, editor of ACC.org & host of Eagle’s Eye View Podcast, and Dr. Devraj Sukul provide the E-CPR and message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai.  

Jump to: Patient summaryCase mediaCase teachingReferences

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Michigan cardiology fellows (Apu Chakrabarti, Jessica Guidi, and Amrish Deshmukh) for some craft brews in Ann Arbor! They discuss a challenging case of Ventricular Septal Rupture after acute MI. Dr. Kim Eagle, editor of ACC.org & host of Eagle's Eye View Podcast, and Dr. Devraj Sukul provide the E-CPR and message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident, Eunice Dugan, with mentorship from University of Maryland cardiology fellow Karan Desai.
D

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Subscribe to our newsletter- The Heartbeat
Support our educational mission by becoming a Patron!
Cardiology Programs Twitter Group created by Dr. Nosheen Reza

Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

Patient Summary

A male in his 60s with medical history of obesity and GERD presents with five days of progressive chest pressure radiating to bilateral arms and associated with dyspnea on exertion. Due to worsening chest pain with new lightheadedness, he decided to come to the ED. His presentation to the hospital was delayed due to fear of contracting COVID-19. In the ED, patient was afebrile, blood pressure 96/56, HR 137, RR 22, and oxygen saturation 94% on room air. On exam, he was ill appearing, acutely distressed, and altered. He had a 3/6 mid systolic murmur loudest at L sternal border, JVP to 10 cm H2O and had crackles up to mid-lung fields. His extremities were cool to touch. Labs notable for Cr 1.5, High-Sensitivity Troponin-T up to 5756, and lactate 3.9. EKG showed incomplete RBBB, PVCs, and ST elevations in the inferior leads with depressions in lateral and precordial leads. Coronary Angiography showed mid-RCA occlusion with faint L to right collaterals. He underwent PCI with restoration of TIMI 3 flow. After PCI, he continued to be hypotensive requiring IABP and norepinephrine. PA catheter demonstrated (in mmHg): RA 26, RV 63/29 (31), 55/36 (44), PCWP 29, and CO 5 L/min, CI 2.2, and SVR 467. Shunt run of mixed venous O2 saturation showed: SVC 71%, RA 72%, RV 62%, PA 85% with oxygen step up in the R-sided circuit. Left ventriculogram then confirmed septal rupture with contrast extravasation from LV into RV. Due to worsening shock, he was stabilized on VA ECMO which was complicated by hemolysis and acute renal failure requiring CVVHD. On day 7 after presentation, he underwent surgery which revealed a large 6×6 cm ventricular septal defect on the posterior aspect of the septum and repaired with a large bovine pericardial path. He was eventually discharged after a prolonged stay and repeat TTE on follow up showed biventricular dysfunction and residual 1cm VSD.  


Case Media

A. ECG: Incomplete RBBB, PVCs, and ST elevations in the inferior leads with depressions in lateral and precordial leads.
B. Coronary angiography: mid-RCA occlusion with faint L to right collaterals.
C-D. A large (6x6cm) VSD was found at the posterobasal aspect of the septum.  Infarcted tissues were removed and a large bovine pericardial patch was used to repair the defect (due to the size of the defect, there was very little viable septum remaining and the patch had to be sewn directly into the LV and RV walls).

LV gram performed showing a left to right shunt.

TEE -1
TEE – 2

Episode Schematics & Teaching


The CardioNerds 5! – 5 major takeaways from the #CNCR case

Coming soon!


References

  1. Birnbaum, Yochai, Michael C. Fishbein, Carlos Blanche, and Robert J. Siegel. “Ventricular Septal Rupture after Acute Myocardial Infarction.” New England Journal of Medicine 347, no. 18 (October 31, 2002): 1426–32.
  2. Goyal, Amit, Menon, Venu. JACC Expert Analysis. Contemporary Management of Post-MI Ventricular Septal Rupture. July 2018. 
  3. Jones, Brandon M., Samir R. Kapadia, Nicholas G. Smedira, Michael Robich, E. Murat Tuzcu, Venu Menon, and Amar Krishnaswamy. “Ventricular Septal Rupture Complicating Acute Myocardial Infarction: A Contemporary Review.” European Heart Journal 35, no. 31 (August 14, 2014): 2060–68.

CardioNerds Case Reports: Recruitment Edition Series Production Team

70. Case Report: Post-MI Free Wall Rupture & Pseudoaneurysm – UCONN

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Connecticut (UCONN) cardiology fellows (Mansour AlmnajamJustice OranefoYasir Adeel, and Srinivas Nadadur) as they enjoy the amazing view from the Heublein tower! They discuss a challenging case of left ventricular free wall rupture & pseudoaneurysm as a complication of a STEMI. Dr. Peter Robinson provides the E-CPR and program director Dr. Joyce Meng provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai.   

Jump to: Patient summaryCase mediaCase teachingReferences

CardioNerds (Amit Goyal & Daniel Ambinder) join University of Connecticut (UCONN) cardiology fellows (Mansour Almnajam, Justice Oranefo, Yasir Adeel, and Srinivas Nadadur) as they enjoy the amazing view from the Heublein tower! They discuss a challenging case of left ventricular free wall rupture as a complication of a STEMI. Dr. Peter Robinson provides the E-CPR and program director Dr. Joyce Meng provides a message for applicants. . Episode notes were developed by Johns Hopkins internal medicine resident Bibin Varghese with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Subscribe to our newsletter- The Heartbeat
Support our educational mission by becoming a Patron!
Cardiology Programs Twitter Group created by Dr. Nosheen Reza

Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

Patient Summary

A man in his mid 50s with no significant PMH presented with a 10-day history of chest pain that progressed to acute pleuritic pain and shortness of breath in the past 24 hours. On arrival, he was hypothermic, in rapid atrial fibrillation with HR in the 130-150s, and an initial BP was not able to be obtained. He was tachypneic with labored breathing, lethargic, and cyanotic. Exam revealed markedly elevated JVP, cool extremities, and diminished breath sounds with bibasilar rales. Labs demonstrated leukocytosis, significantly elevated liver enzymes, troponin-I at 10.91, elevated NT-proBNP, and lactate at 6. ECG demonstrated tall, broad R-waves in V1-V4 with downsloping STD and upright T-waves concerning for a posterior infarct. He was immediately intubated, cardioverted into NSR, and started on vasopressors. Bedside echocardiogram demonstrated diffuse LV hypokinesis with akinesis of the inferolateral wall, LVEF 25-30%, and pericardial fluid with hyperechoic material adherent to the inferior wall as well as tamponade physiology. Chest CTA was negative for aortic dissection and confirmed hemopericardium. He was taken to the OR where he underwent a subxiphoid pericardial window. They found significant clot burden (both old and new), but no frank rupture. Adherent clot was not removed to prevent further hemodynamic compromise. Intraoperative TEE additionally demonstrated severe eccentric MR with partial posteromedial papillary muscle rupture. An IABP was placed and inotropic and vasoactive support was continued to temporize pending definitive therapy and the patient improved hemodynamically. Repeat TTE prior to surgery demonstrated a large apical and inferolateral pseudoaneurysm. Coronary angiogram revealed proximal occlusion of the LCx and diffuse three vessel coronary disease otherwise. He ultimately underwent CABG, mechanical mitral valve replacement, and pericardial patch repair of the ventricular pseudoaneurysm. Final diagnosis: Free Wall Rupture & Pseudoaneurysm. Thankfully, the patient ultimately made a complete recovery!  


Case Media

A. ECG: tall, broad R-waves in V1-V4 with downsloping STD and upright T-waves
B. CXR
C. CT angiogram thoracic aorta: Moderate sized hemopericardium with tamponade physiology. Transmural infarction of LV base to mid inferior wall. Circumflex occlusion just beyond the first obtuse marginal. Normal aorta without dissection or aneurysm.
D-F. Coronary angiogram: LCx is occluded proximally, distal vessel fills via faint collaterals from the right, OM1: Fills via right to left collaterals. LAD: 70%, mid; 90%, apical, 1st diagonal: 50%, ostial; 60-70%, proximal; 90% of inferior subdivision, bifurcating vessel. RCA: (Dominant); 50%, mid: 40%, distal. PDA: 60%, proximal, small-caliber vessel. PLV: 60-70%, proximal


TEE: Trans-gastric views
TEE
TEE: MV with color
CORS: Occluded Lcx
CORS: Obstructive CAD in LAD
CORS: RCA
TTE: PLA
TTE: A4C
TTE: A4C with contrast demonstrating an LV pseudoaneurysm

Episode Schematics & Teaching


The CardioNerds 5! – 5 major takeaways from the #CNCR case

  1. This patient presented with EKG showing a posterior myocardial infarction. Why was he not taken to the cath lab immediately for revascularization? 
    • Duration of ischemia, its relationship to infarct size, and the mortality benefit from reperfusion therapies are crucially related to time in the very early course of STEMI. However, this relationship breaks down in patients presenting late after a STEMI. 
    • In OAT (Occluded Artery Trial), hemodynamically stable patients who presented late (3-28 days) after a myocardial infarction with high risk features (e.g., proximal LAD occlusion with TIMI 0 to 1 flow) were randomized to PCI + optimal medical therapy (OMT) within 24 hours or OMT alone. There was no difference in the primary endpoint of all-cause mortality, nonfatal MI, or NYHA class III to IV heart failure. These findings are reflected in the ACC/AHA guidelines, where delayed PCI of a totally occluded infract artery >24 hours after STEMI in hemodynamically and electrically stable patients is given a Class III recommendation (no benefit).  
    • Although the patient presented with EKG findings concerning for a posterior STEMI, this was likely 10 days after his acute insult. In addition, his hemodynamic instability and bedside POCUS raised the concern for a mechanical complication of a STEMI. In a patient with suspected mechanical complication of acute MI, such as free wall rupture and acute MR, the priority of therapy is to rapidly identify the mechanical problem and perform emergency surgical therapy. Furthermore, the need for antiplatelet therapy following any PCI would complicate surgical planning.  
    • PCI may be helpful in patients with ischemia induced papillary muscle dysfunction (“ischemic MR”). However there is no role for immediate PCI when the mechanical integrity of the mitral valve has been compromised. 
  2. This patient presented with hemodynamic instability and bedside POCUS revealed pericardial fluid with tamponade physiology. What are some causes of acute hemorrhagic pericardial effusion? 
    • When thinking about hemorrhagic pericardial effusions, expedited evaluation is critical. While there is overlap with traditional causes of pericardial effusion, some causes may need immediate intervention. Amongst these considerations are iatrogenic complication of cardiac surgery, cardiac catheterization, or electrophysiologic procedures. Other etiologies include complications of myocardial infarction including free wall rupture/pseudoaneurysm, complication of aortic dissection, and trauma. As with serous pericardial effusions, malignancy should remain on the differential, as well as tuberculosis in endemic areas.  
  3. A CTA of the aorta ruled out dissection but showed a moderate sized hemopericardium raising concern for a mechanical complication of posterior MI, specifically a free wall rupture (FWR). What are the risk factors for a FWR after an MI? 
    • Ventricular free wall rupture is quite uncommon in the reperfusion era; however, if it does occur, mortality rates are high. FWR typically occurs acutely or sub-acutely, occurring within 2 weeks for 90% of patients. Risk factors include first myocardial infarction, poor collateralization of the infarcted territory, older age, female sex, persistent ST elevation and delayed presentation/unsuccessful revascularization. When patients present acutely, patients will typically develop tamponade, rapidly progress to pulseless electrical activity, and/or  sudden cardiac death. When patients develop subacute FWR or contained rupture (i.e., pseudoaneurysm), they may present with signs and symptoms of pericarditis and subacute hypotension. 
    • When FWR occurs, it typically involves the anterior, posterior, or lateral left ventricular wall. The pathophysiology of ventricular free wall rupture is related to the timing of the rupture. Rupture will typically occur at the border of the necrotic and healthy (and often hyperkinetic) myocardium and in areas of the greatest shear stress. In the left ventricle, this tends to be near the anterior and posterior papillary muscles, regardless if they are compromised in the infarct. 
    • Note, pericardial effusions can be a common finding in the setting of an acute MI (~15-25% of patients in the acute setting); however, a rapidly expanding pericardial effusion associated with significant wall thinning along the infarcted region should raise the suspicion for LV free wall rupture.  
  4. The patient was stabilized after surgical evacuation of pericardial fluid in the OR. When should you consider pericardiocentesis vs surgical management? 
    • In cases of cardiac tamponade with concern for circulatory collapse there are no absolute contraindications to pericardiocentesis. The goal is urgent drainage of pericardial fluid and how we drain the fluid will depend on the etiology, acuity, and available providers. Emergent surgical management should generally be considered first line in patients with traumatic hemopericardium, aortic dissection related hemopericardium, or free wall rupture. In the setting of aortic dissection, controlled drainage of very small amounts of hemopericardium can be considered as a temporizing measure to maintain SBP > 90 mmHg. With purulent or loculated effusions, surgical drainage over pericardiocentesis may be the preference as well.  
    • Supportive measures include ensuring adequate preload, avoiding diuretics and/or vasodilator therapy, and inotropic and vasopressor therapy as needed.  
  5. The patient was found to have a pseudoaneurysm rather than a frank free wall rupture. What is a pseudoaneurysm and how is it different than a true ventricular aneurysm? 
    • Ventricular pseudoaneurysm is caused by a contained rupture of the LV free wall where the rupture is contained by adherent pericardium, thrombus, or hematoma with no myocardial tissue in the outpouching. In a true ventricular aneurysm, the outer walls are formed by the infarcted myocardium and scar tissue. Pseudoaneurysms have a high propensity to rupture and thus surgical management is recommended.  
    • A small, narrow neck typically connects the ventricular cavity with the contained pericardial space. On echocardiogram, pseudoaneurysm can demonstrated the following differentiating features: (1) neck diameter to maximal aneurysmal diameter < 0.5; (2) color and spectral doppler demonstrating bidirectional flow through the narrowed neck; (3) thrombus and/or spontaneous echo contrast in the pericardial space.  

References

  1. Alkhalil Mohammad, Choudhury Robin P. Reperfusion Treatment in Late Presentation Acute Myocardial Infarction. Circ Cardiovasc Interv. 2018;11(9):e007287. doi:10.1161/CIRCINTERVENTIONS.118.007287 
  2. Hochman JS, Lamas GA, Buller CE, et al. Coronary Intervention for Persistent Occlusion after Myocardial Infarction. N Engl J Med. 2006;355(23):2395-2407. doi:10.1056/NEJMoa066139 
  3. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseasesThe Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015;36(42):2921-2964. doi:10.1093/eurheartj/ehv318 
  4. Hutchins KD, Skurnick J, Lavenhar M, Natarajan GA. Cardiac rupture in acute myocardial infarction: a reassessment. Am J Forensic Med Pathol. 2002 Mar;23(1):78-82. doi: 10.1097/00000433-200203000-00017. PMID: 11953501. 
  5. Griffin, Brian P. 2019. Manual of cardiovascular medicine. 

CardioNerds Case Reports: Recruitment Edition Series Production Team

64. Case Report: RV Infarction Treated with RVAD Support – Houston Methodist

CardioNerds (Amit Goyal & Daniel Ambinder) join Houston Methodist cardiology fellows (Isaac Tea, Stephanie Fuentes, Peter Rothstein) for a trip to Hermann Park! They discuss a challenging case of right ventricular (RV) infarction leading to acute RV failure treated with right ventricular assist device (RVAD) support. Dr. Mahwash Kassi provides the E-CPR and program director Dr. Stephen Little provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai

Jump to: Patient summaryCase mediaCase teachingReferences

CardioNerds (Amit Goyal & Daniel Ambinder) join Houston Methodist cardiology fellows (Isaac Tea, Stephanie Fuentes, Peter Rothstein) for a trip to Hermann Park! They discuss a challenging case of right ventricular (RV) infarction leading to acute RV failure treated with right ventricular assist device (RVAD) support. Dr. Mahwash Kassi provides the E-CPR and program director Dr. Stephen Little provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

CardioNerds Case Reports Page
CardioNerds Episode Page
CardioNerds Academy
Subscribe to our newsletter- The Heartbeat
Support our educational mission by becoming a Patron!
Cardiology Programs Twitter Group created by Dr. Nosheen Reza

Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

Patient Summary

A man in his early 70s with ASCVD risk factors and known CAD (PCI to proximal LAD 4 years prior) presented with typical angina refractory to maximal medical therapy. A nuclear stress test showed a reversible perfusion defect in the RCA territory, and he was referred for PCI. Coronary angiogram showed severe stenosis of the proximal RCA and a DES was successfully deployed with TIMI 3 flow, though several large acute marginal branches were jailed.  

The night following PCI, the patient developed bradycardia, hypotension, and tachypnea. Physical exam showed newly elevated JVP, lower extremity edema, and bibasilar crackles without a new cardiac murmur. ECG showed ST elevation in V1-V4, and bedside echocardiogram showed a severely dilated RV with decreased systolic function. With concern for acute RV failure, the patient was fluid resuscitated, started on dopamine for chronotropy, and was admitted to the CCU. A Swan-Ganz catheter was placed, showing a CVP 12, RV 41/15, PA 36/20 (25), PCWP 18, CI 1.6 (by Fick method). The calculated PAPi was 0.84.  

The patient was transitioned to dobutamine to improve RV inotropy, epinephrine in the setting of hypotension, and inhaled nitric oxide in an attempt to decrease RV afterload. Despite these interventions, the patient had worsening shock, anuric renal failure requiring CVVH, and respiratory failure requiring intubation. A centrifugal RA to PA pump was placed (Protek Duo) for right-sided mechanical circulatory support, with improvement in RV hemodynamics and cardiogenic shock. Notably, a repeat angiogram was done, which showed a patent left coronary circulation as well as a right coronary artery without flow in the acute marginal branches. After 6 days of mechanical circulatory support, the patient was ultimately able to be weaned from vasoactive agents, and the Protek Duo was removed. He continued to have junctional bradycardia, and a permanent pacemaker was placed. After a nearly month-long admission, the patient was discharged to rehab; at 4 months follow-up, the patient’s RV function had improved on TTE, and he was not limited from heart failure symptoms.  


Case Media

A: ECG, initial
B: ECG: 8 hours post PCI he was noted to have junctional bradycardia with ST-segment elevations in V1-V4.
C: Pre and post RCA PCI
D: TTE: EF 50-55%, Severely enlarged RV with severely reduced systolic function, TAPSE 1.4 cm, Myocardial systolic excursion velocity (S’): 5.9
E: CXR- shock
F: Swan, Protek Duo Cannula, Temporary pacer
G: CXR and TTE images demonstrating Protek Duo cannula placement

Left Coronary System -1
Left Coronary System – 2
Severe eccentric serial stenoses in the proximal to mid RCA – 1
RCA – 2
RCA PCI – 1
RCA PCI – 2
RCA PCI – 3
RCA PCI – 4

RCA – Final
TTE -1
TTE -2
Repeat angiogram: Patent stents, sluggish flow
Protek Duo Placement

Episode Schematics & Teaching


The CardioNerds 5! – 5 major takeaways from the #CNCR case

1) Don’t forget about the RV, because it sure won’t forget about you! Cardionerds, how do you break down the pathophysiology of acute RV failure? 

  • Understanding the pathophysiology of RV failure requires a basic understanding of RV physiology. Normal RV function depends on systemic venous return, RV afterload, pericardial compliance/constraint, and native RV contractility. Remember, the thin-walled RV requires much less energy to generate output compared to the LV as the RV is pumping into the highly compliant, low-resistance pulmonary circulation. Overall, the RV is highly sensitive to changes in RV afterload. 
  • Thus, when we think of acute RV failure, our primary considerations are factors that rapidly increase RV afterload (e.g., pulmonary embolus), as well as conditions with decreased RV contractility (e.g., RV ischemia). The RV is more adept to tolerating changes in volume rather than pressure (since it is coupled to the low-resistance, high compliance pulmonary circulation). Contrast this with the LV, which tolerates changes in pressure more than volume. An acute increase in RV afterload can abruptly precipitate a fall in RV cardiac output! 
  • With an acute decreased in RV contractility (e.g., RV infarct), the RV can dilate leading to functional TR; this can further exacerbate RV dilation, leading to impaired LV filling due to ventricular interdependence. As the septum shifts leftward, this can impair LV filling by increasing LVEDP and lead to hypotension. Direct RV injury can promote more RV injury/ischemia, as elevated right heart pressures can cause coronary sinus congestion reducing coronary blood flow and leading to more RV ischemia. 
  • For more detailed explanation of Right-Sided Heart Failure, see this fantastic Scientific Statement from the AHA! 

2) Lets focus on ischemic RV disease: what is the coronary supply to the RV, and how does coronary blood flow to the RV differ than that of the LV? 

  • Compared to the LV, the RV is more resistant to irreversible ischemia. Coronary blood flow to the RV occurs both in systole and diastole, RV myocardial oxygen demand at rest is lower than that of the LV with smaller muscle mass, and there is often extensive collateral circulation from the left coronary system. However, RV coronary perfusion pressure can decrease rapidly in the setting of systemic hypotension and increased RV intracavitary pressure.  
  • In most patients, the RV is supplied by the RCA via RV acute marginal branches largely supplying the anterior RV free wall. Significant RV involvement in an RCA culprit acute myocardial infarction tends to only occur if the occlusion is proximal to the acute marginal branch. Furthermore, the extent of RV involvement may be attenuated by the amount of left to right collateralization.  
  • Note, the LAD supplies the RV apex, as well as a portion of the RV anterior wall that is contiguous with the anterior septum. Notably, in patients with a left dominant coronary system or in patients with a chronically occluded RCA with extensive left to right collateral flow, more than half of the RV free wall may be supplied by the left system. 

3) Now that we know what causes acute RV failure, what can we do to assess for acute RV failure, both at the bedside and with advanced diagnostics? 

Physical exam: In acute RV failure, we will likely see elevated neck veins +/- Kussmaul’s sign, hypotension, possibly clear lungs depending on etiology, and tricuspid regurgitation murmur. Enjoy Ep #58 – Constrictive Pericarditis CN5 for more details on right-sided exam findings! 

ECG: Unfortunately, the standard 12-lead ECG provides limited definitive information on RV failure. However, we should evaluate for acute occlusive myocardial infarction (MI) involving the RV, including ST elevation in the inferior leads (classically with III > II), V1 > V2, and/or V1 +/- ST depression in V2. Right-sided leads can further confirm acute occlusive MI, with STE > 1mm in lead V4R sensitive and specific for RV infarct. With a large RV infarct, we may see brady-arrhythmias. Other signs of acute RV failure may include RV strain pattern (e.g., ST depression and T wave inversions in V1-V3). Enjoy Ep #60 – Massive PE for more on ECG changes in acute PE and RV failure! 

CT: While usually not obtained in the setting of acute RV failure unless evaluating for acute PE or parenchymal lung disease, RV:LV ratio >1.0, pulmonary trunk enlargement, and contrast reflux into the inferior vena cava and hepatic veins suggest right heart failure. A gated cardiac contrast-enhanced CT can provide more information about chamber size/function and valvular pathology. 

TTE: Echo is crucial in the diagnosis of RV failure! One of the first things to pay attention to is RV size, with RV dilation being a poor prognostic sign; RV:LV ratio > 1 is associated with increased in-hospital mortality in some studies of acute PE patients. Evaluate the position of the interventricular septum, which may be flattened in systole suggestive of RV pressure overload and/or in diastole suggestive of volume overload. RV systolic function can be assessed by tricuspid annular plane systolic excursion (TAPSE) which is a marker of longitudinal myocardial shortening with abnormal being less than 1.6 cm. There are limitations to use of TAPSE, but it remains a relatively specific test for RV dysfunction. An estimation of pulmonary artery systolic pressure (PASP) should be done utilizing the TR jet; however, in the setting of severe TR, the doppler envelope is often low velocity and early peaking because of high RA pressure making PASP difficult to estimate. The IVC should be evaluated for size, response to respiration and hepatic vein reversal. There are many more aspects to review regarding acute RV failure and RV systolic function like fractional area change, tissue doppler velocity, and RV strain (see the references below!), but also remember to evaluate for specific pathology, including signs of acute PE such as McConnell’s sign. 

RHC: In the setting of acute right heart failure, a right heart catheterization may be necessary to guide therapy. An elevated right atrial pressure, and specifically an elevated right atrial pressure to pulmonary capillary wedge pressure ratio can be indicative of right heart failure; the specific ratio depends on disease state, but generally >0.6 to 0.8 suggestive of RV failure. PA pulsatility index (PAPi) has become a useful tool in evaluating for RV failure specifically in the setting of acute myocardial infarction. An abnormal value depends on disease state as RV pulsatility is not only a function of RV function, but also pulmonary vascular resistance and capacitance. 

4) So, what’s the big deal? How does acute RV failure cause shock? 

  • Decreased RV cardiac output, combined with a dilated RV, leads to interventricular septal shift towards the left, compromising LV filling (preload) as discussed above. Decreased LV preload eventually leads to decreased LV cardiac output and hypotension, causing end-organ damage and decreased coronary perfusion. Elevated right-sided filling pressures with systemic venous congestion can lead to hepatic and renal congestion, exacerbating fluid retention. Decreased coronary perfusion can leads to decreased oxygen delivery to a failing RV that already has a higher oxygen demand (due to increased RV afterload and wall tension). This, ultimately can cause further RV ischemia and collapse in RV function. This physiologic phenomenon is referred to as the RV Spiral of Death.  

5) Yikes! What can we do to break this spiral and medically manage RV failure? Is there a role for mechanical support? 

  • Correct the initial insult to the RV! As we take measures to support the RV, we have to ensure we evaluate for the etiology of RV failure and treat the underlying cause. This includes PCI in the setting of RVMI, anticoagulation/thrombolysis/thrombectomy in the setting of PE, and medical management in the setting of sepsis! 
  • Address preload! Remember, not all RV failure is created alike. An acute RV infarct may be highly pre-load dependent and may need fluid boluses. However, depending on the underlying pathology, excessive preload may be detrimental, leading to excess wall stress and RV dilation, which can potentially exacerbate left-ward septal shift and impede LV filling. Ventricular interdependence as a result of RV dilation and pericardial constraint may play a larger role in worsening acute RV failure than decreased RV ejection fraction, and thus decompression of the RV is necessary (e.g., diuretics, renal replacement therapy), as guided by exam +/-  RHC. 
  • Reduce RV afterload! First, address reversible factors leading to pulmonary vasoconstriction including hypoxia and acidosis. In patients receiving positive pressure ventilation, PEEP should be optimized to avoid atelectasis, while also avoiding over distension of alveoli and worsened RV afterload. Non-selective systemic vasodilators (e.g., intravenous sodium nitroprusside > nitroglycerin) decrease systemic and pulmonary vascular resistance, and thus decrease LV and RV afterload. Selective pulmonary vasodilators, such as inhaled nitric oxide and epoprostenol can also be effective in specific patient populations.  
  • Improve Contractility and Maintain PerfusionDobutamine and milrinone both improve RV inotropy at the cost of arrhythmogenicity. Both agents can also lead to vasodilation and thus whether hypotension worsens may depend on how effectively these agents assist in augmenting LV preload compared to systemic vasodilation. In the setting of hypotension, combined vasopressor and inotropic medications may be needed including norepinephrine and/or epinephrine. With escalating doses of vasoactive medications, vasopressin may be needed to maintain end-organ perfusion.  
  • Assess chronotropy! RV infarcts increase the risk of bradycardia and AV block. Temporary pacing may be necessary in these patients.  
  • In refractory acute RV failure, consider mechanical support! There are 3 main options for temporary RV mechanical support:  
    • VA-ECMO substantially reduces RV preload and afterload, though it can dramatically increase LV afterload VA ECMO is an indirect way to bypass the RV compared to MCS below.  
    • RA to PA extracorporeal pump (ex. Protek Duo and Tandem Heart RVAD) removes blood from the RA and delivers it into the PA using a centrifugal pump and an oxygenator can be added if needed. RV preload is reduced while increasing mean PA pressure and LV preload. 
    • Micro-axial flow device (e.g., Impella RP) with an inflow in the RA and an outflow in the PA. 

References

  1. Koo, B. K., Kang, H. J., Youn, T. J., et al. (2005). Physiologic assessment of jailed side branch lesions using fractional flow reserve. Journal of the American College of Cardiology, 46(4), 633–637. 
  2. Fincke, R., Hochman, J. S., Lowe, A. M., et al. (2004). Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. Journal of the American College of Cardiology, 44(2), 340–348. 
  3. Kapur, N. K., Esposito, M. L., Bader, Y., et al. (2017). Mechanical Circulatory Support Devices for Acute Right Ventricular Failure. Circulation, 136(3), 314–326.  
  4. Konstam, M. A., Kiernan, M. S., Bernstein, D., et al. (2018). Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association. Circulation, 137(20), e578–e622.  
  5. Jeffers JL, Boyd KL, Parks LJ. Right Ventricular Myocardial Infarction. [Updated 2020 Aug 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK431048/ 
  6. Sanz, J., Sánchez-Quintana, D., Bossone, E., et al. (2019). Anatomy, Function, and Dysfunction of the Right Ventricle: JACC State-of-the-Art Review. Journal of the American College of Cardiology, 73(12), 1463–1482.  
  7. Korabathina, R., Heffernan, K. S., Paruchuri, V., et al. (2012). The pulmonary artery pulsatility index identifies severe right ventricular dysfunction in acute inferior myocardial infarction. Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions, 80(4), 593–600.  

CardioNerds Case Reports: Recruitment Edition Series Production Team

51. Case Report: Embolic Acute Coronary Syndrome from PFO & Pulmonary Hypertension – Lankenau Medical Center

CardioNerds (Amit Goyal & Dan Ambinder) join Lankenau Medical Center cardiology fellows (Gwen McNeill and Shaung Ooi) for some Philly cheesesteaks! They discuss a fascinating case of Embolic Acute Coronary Syndrome from PFO and Pulmonary Hypertension. Dr. John Clark provides the E-CPR and program director Dr. Jeanine Romanelli provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai

Jump to: Patient summaryCase figures & mediaCase teachingEducational videoReferencesProduction team

CardioNerds (Amit Goyal & Dan Ambinder) join Lankenau Medical Center cardiology fellows (Gwen McNeill and Shaung Ooi) for some Philly cheesesteaks! They discuss a fascinating case of Embolic Acute Coronary Syndrome from PFO and Pulmonary Hypertension. Dr. John Clark provides the E-CPR and program director Dr. Jeanine Romanelli provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.
Episode graphic by Dr. Carine Hamo

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

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Cardionerds Cardiology Podcast Presents CardioNerds Case Report Series

Patient Summary

A woman in her early 40s with history of tobacco and prior methamphetamine use presented with acute onset chest pain. She was found to have an elevated troponin, anterior T wave inversions, and apical akinesis on TTE. Coronary angiography showed a coronary embolism in the mid-distal LAD. Attempts to wire the lesion led to distal embolization of the clot, and IVUS showed no underlying arteriosclerosis.  

To investigate the etiology of the coronary embolus, a repeat TTE with agitated saline was done that suggested a PFO with right to left flow, as well as decreased RV function with an estimated RVSP of 70 mmHg. The clinical picture was that of a paradoxical coronary embolus, arising from the right (venous) side traveling to the left (arterial) side via a PFO. PFO closure was discussed but not performed given severe pulmonary hypertension with Right to Left shunt. In this circumstance, the PFO functions as a “pop-off valve” for the overloaded RV; closing it risks precipitating acute RV overload and failure. A RHC showed a PA pressure of 70/24 mmHg with mPAP of 40 mmHg, PCWP 5 mmHg, and PVR of 11 woods units. Given concern for idiopathic PH, a vasodilator challenge was done which did not show reactivity, and she was started on ambrisentan and sildenafil. Ultimately, the etiology of her pulmonary hypertension was felt to be due to PAH from prior methamphetamine use vs. idiopathic PAH. On follow-up, her PA pressures and RV function had greatly approved, allowing for safe and successful PFO closure in an attempt to prevent future emboli.  Final diagnosis: Embolic Acute Coronary Syndrome from PFO & Pulmonary Hypertension.


Case Media

1. Coronary angio of embolism
2. PFO on TEE with R to L shunt by Doppler
3. TTE bubble after PFO closure

Episode Schematics & Teaching


The CardioNerds 5! – 5 major takeaways from the #CNCR case

  1. Coronary emboli are an uncommon cause of myocardial infarction. We can think of the etiology of coronary emboli in three major categories: Direct, Paradoxical, or Iatrogenic. 
    1. Direct emboli originate from the left side of the heart: sources include clot (from atrial appendage, apical thrombus), valvular lesion (vegetation, thrombus, fibroelastoma), or left sided cardiac mass (atrial myxoma, rhabdomyosarcoma). 
    2. Paradoxical emboli originate from the right side or systemic venous circulation, and pass from right to left through an atrial septal defect, patent foramen ovale, or pulmonary arteriovenous malformation. 
    3. Iatrogenic emboli occur following procedures such as valve replacement or PCI. Note that iatrogenic is the most common etiology! 
  2. PFOs are present in up to 25% of adults, but are usually clinically insignificant. However, there is increasing evidence that PFO closure is moderately beneficial compared to antiplatelet therapy alone in patients less than 60 years old with cryptogenic, non-lacunar ischemic stroke. PFO closure may particularly benefit those with a large right-to-left shunt or an associated atrial septal aneurysm.
  3. Remember closing an ASD in the setting of significant pulmonary hypertension can lead to decompensation, as the interatrial connection may be serving as a “pop-off” valve to decompress the RV and maintain cardiac output in the setting of high PA pressures! Specifically, ASD closure is generally contraindicated if the PA systolic pressure is > 2/3 systolic blood pressure, pulmonary vascular resistance > 2/3 systemic vascular resistance, or if  a net right-to-left shunt is present. 
  4. Recall that the hemodynamic definitions of pulmonary hypertension changed in 2019. A mean pulmonary artery pressure of 20 or greater confirms a diagnosis of pulmonary hypertension. A PCWP ≤15 mmHg with pulmonary vascular resistance ≥3 woods units suggests pre-capillary pulmonary hypertension, while a PCWP >15 with pulmonary vascular resistance <3 woods units suggests isolated post-capillary PH.  
  5. During a right heart catheterization, a pulmonary vasodilator challenge can be done to identify vasoreactive patients who may respond to calcium channel blockers. This is typically recommended for idiopathic and hereditary PAH. A positive response is defined as a drop in mean PAP to <40 mmHg, with a decrease of at least > 10 mmHg, with unchanged or increased cardiac output. These patients can be started on amlodipine or nifedipine, but should be followed closely as they may not always remain vasoreactive and clinical deterioration is possible! 

Educational Video

Produced by Dr. Karan Desai

References


CardioNerds Case Reports: Recruitment Edition Series Production Team