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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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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.  

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Case Media

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Episode Schematics & Teaching

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

Classification and Management of Post-AMI VSR 

Why and in whom should we worry about VSR? 

• Ventricular Septal Rupture or VSR is rare in the era of early reperfusion strategies. Historical incidence of VSR after AMI was thought to be 1-2% and has decreased to between 0.17% and 0.3%. It can be attributed to early identification and restoration of flow in the infarct related artery (IRA). Although the incidence has decreased, the mortality remains high (41-80%). 
• Risk factors include older age, female sex, history of heart failure, and chronic kidney disease. If VSR does occur it tends to be in a patients presenting with their first MI with delayed, failed or no reperfusion therapy. The presence of collaterals is likely protective against developing VSR and reducing size of infarct.  

How do we recognize and diagnose VSR after AMI? 

• Abrupt hemodynamic compromise after revascularization or refractory shock with AMI should prompt suspicion for mechanical complications, including VSR. Note: some patients may be stable early in their course.  
• The classic presentation would be recurrent chest pain and hypotension several days after an MI, along with a new harsh holosystolic murmur usually best heard at the left lower sternal border sometimes accompanied by a thrill. Identifying this murmur requires a thorough baseline examination and frequent re-evaluation. Note, the absence of this murmur does not rule out VSR as the murmur may not be audible in a large VSR. 
• In terms of making the diagnosis of VSR, TTE is the starting point. The location of the VSR will likely depend on the infarct related artery (see below), but the two most common locations are basal inferoseptal and anteroapical septal walls. To identify the VSR it is critical to use color doppler in the area of interest and to lower the Nyquist limit to readily identify lower velocity flow with better definition.  
• TTE is also critical to define worsening pulmonary hypertension and/or left and right ventricular dysfunction as these are prognostic factors. When there are poor image quality and the defect cannot be readily identified, TEE may be necessary.  
• If a RHC is available, we can identify a left to right shunt via an oxygen step-up. Normal oxygen saturation in the RV is typically 64 to 68%. When there is an increase in oxygen saturation from RA to RV (or PA) of greater than 5% that can be suggestive of a VSR. Further, we can calculate the shunt fraction to quantify the extent of the shunt. 
• During a left heart catheterization, LV ventriculography can identify the VSR 

When does VSR occur post AMI and how does IRA relate to VSR location? 

• It is historically thought to occur between 3-6 days after AMI, however newer studies show earlier development with one study showing median time of 16 hours after AMI. This may be related to more awareness, increased access to echo, or a change in the presentation of VSR due to earlier reperfusion strategies. 
• The LAD and the RCA are the arteries most commonly implicated in the development of a VSD. Remember, anatomically, the LAD supplies the apical portion of the ventricular septum and the RCA gives posterior septal perforators that supply the basal inferoseptal wall. These areas are the most common locations for VSR after a transmural infarct as they are located at the border zone of a myocardial infarct.  
• Remember the defect can be simple or complex. A complex VSR is associated with multiple areas and various dissection planes that track along the myocardium.  

What is the pathophysiology and classification for VSR 

• We can classify VSR in 2 ways: the Becker and Mantgem system and simple vs. complex.  
• The Becker and Mantgem system was originally made for cardiac free wall rupture, but is also used for pathological classification of VSR. There are 3 mechanisms and pathophysiologic findings that correlate with temporal presentation. 
  • Type 1 : Occurs acutely (<24 hr) and are abrupt slit-like tear associated with infarcts without wall thinning. 
  • Type 2: Occurs sub-acutely (>24 hours) typically shows slow erosion of infarcted myocardium due to neutrophilic infiltration of ischemic/necrotic tissue 
  • Type 3:  Occurs late following an MI and after aneurysm formation and then subsequent rupture 
• In the simple vs. complex VSR classification, we classify VSR as simple if there is a direct connection between the LV and RV. Meanwhile, a complex VSR is a serpiginous connection (multiple planes) and more likely caused by hemorrhage. 

What are the goals of management and definitive therapy? 

• Surgical repair is the ideal definitive treatment, though mortality is very high. Patients with worse outcomes after surgery are female, older, RV dysfunction and have higher level of cardiac circulatory compromise.  
• Newly infarcted tissue is weak and friable, may not hold sutures well, and is prone to repeat defects. Successful repair requires complete debridement of necrotic tissue and sparing of healthy tissue which may be difficult to differentiate in the early stages after infarction. Surgical mortality appear to be higher with basal inferoseptal rupture associated with inferior MI, as these patients may need concomitant mitral valve repair as they often have ischemic MR as well 
• Timing of surgery is a complex issue and there are no clear guidelines for timing of surgery and therefore it is an individualized decision. Studies show that patients who were able to wait >7 days after VSR for repair had a lower mortality compared to <7 days likely due to improved cardiac tissue stability, but survival bias could play a major role here. Although the mortality with repair is high, non-surgical mortality is even higher. Patients who didn’t undergo surgery by day 30 had a 94% mortality rate.   
• While awaiting surgical repair, the goal of medical management is afterload reduction to reduce shunt fraction. This can be accomplished with IV medications (e.g., nitroprusside) or IABP. Other MCS as a bridge can be considered, including ECMO, Tandemheart, and total artificial heart. Percutaneous closure is an option as a bridge or definitive treatment for those with high surgical risk, but need to consider factors such as size of rupture and viable septal muscle.  
• Residual or recurrent VSR after surgical repair can be seen in up to 28% of surviving patients. If asymptomatic, it can be treated conservatively. However, in patients with clinical heart failure or Qp/Qs >2 (significant left to right shunt), repeat repair may improve outcomes. 

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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.

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CardioNerds Case Reports: Recruitment Edition Series Production Team

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