Magnus-DRAFT (KG- Done) - Dysnea-80yom (1-13.1-2025)-DRAFT- I_am_DONE

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MY Comment, by KEN GRAUER, MD (1/14/2025):

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I found today's case highly insightful with regard to many aspects. These include:

• The fact that although serious complications from acute MI are far less common than in years past — today's case manifests a "combination" of post-infarct complications (ie, post-MI pericarditis; post-MI VSR = Ventricular Septal Rupture). Awareness of the course of these complications is important to facilitate earlier detection.
• This patient's MI was in large part "silent" — in that CP (Chest Pain) was not a prominant complaint. Instead, the patient's primary symptom was severe dyspnea (See the September 5, 2024 post in Dr. Smith's ECG Blog regarding the frequency of "silent" MI, especially in older patients who present with acute dyspnea — with that Sept. 5 case also from Dr. Nossen, and also associated with post-MI VSR). 
• Physical Exam was revealing. Most of the time with acute MI — little additional information is provided by physical examination (with exception of those acute MI patients who present with heart failure or shock). Today's patient presented with a harsh, holosystolic murmur consistent with acute VSR. This was detected on admission through the ED (Emergency Department) — but we are not provided with information as to whether a murmur was detected 4 days earlier when the patient was seen in an ambulatory care center and treated with antibiotics for pneumonia. This is relevant — as knowing when the murmur appeared may have expedited realization of VSR in this elderly patient with dementia and severe dyspnea.
• We are not told if a pericardial friction rub was listened for. This could have been another clue for facilitating earlier recognition of tihs patient's post-event pericarditis.
• Point of care Echo was diagnostic — showing obvious regional wall motion abnormality of the distal septum and ventricular apex. Once again, earlier use of Echo would have expedited recognition of the cause of this patient's dyspnea that began 6 days earlier.
• Finally — No ECG was apparently done 4 days earlier at the time of the primary care visit. I learned by subsequent history that this initial encounter was a home visit by a primary care provider — with assessment clearly challenging because of the patient's dementia. But in the "retrospectoscope" — I find it insightful to look back and contemplate whether the patient should have been sent to the ED for evaluation at that time. This is not in any way a criticism — since we clearly lack details for any judgment. But we learn from cases that don't go as expected (ie, it appears the patient never had pneumonia) — and doing the "hard work" of considering what we might do differently the next time we encounter a similar situation is how we improve as clinicians.
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• P.S.: There is no mention of a prior ECG in today's case. Realizing that we are not privy to many of the details in today's case — locating a prior tracing for comparison may have clarified a number of conflicting findings in today's ECG (that I've reproduced and labeled in Figure-1).

QUESTION:

• How would you interpret the ECG in Figure-1?

Figure-1: I've labeled the initial ECG in today's case.

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NOTE:  The ECG in Figure-1 was initially recorded using the Cabrera Format — in which both the recording speed and limb lead sequencing have been altered (ie, Rather than +aVR — the negative display of lead aVR is used = -aVR).

• Because my "ECG brain" has been wired for interpretation of ECGs at the 25 mm/second speed (that is standard in the U.S. and in most of the world) — My routine is to selectively reduce the width of such tracings by 50% to compensate for the 50 mm/second speed routinely used with the Cabrera format. This has been done in Figure-1. 
• Outlined in BLUE just above lead V1 — are several ECG grid boxes to facilitate recognizing that the R-R interval in ECG #1 is slightly more than 3 large boxes in duration — corresponding to sinus rhythm at a rate of ~90-95/minute.
• Given globalization of our world — we favor familiarization with different recording formats (For detailed review of the Cabrera Format — Check out My Comment at the bottom of the page in the October 26, 2020 post in Dr. Smith's ECG Blog).

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The ECG in Figure-1:

As noted — there is sinus rhythm at ~90-95/minute. The PR interval is normal. The QRS is not wide. 

• The QTc appears to be at the upper limit of normal, or borderline prolonged (Using our QTc Calculator described in the January 12, 2025 post — and plugging in a rate of ~95/minute and a measured QT = 370 msec, as seen in leads V3,V4 — we come up with an estimated QTc clearly under 450 msec., or still normal).
• Although mid-precordial S waves are quite deep — voltage criteria for LVH are not quite met (See My Comment in the June 20, 2020 post). Instead, the deep chest lead S waves are probably the result of a lack of opposing forces from extensive anterior infarction.

There are Q waves:

• Multiple Q waves are seen. Although narrow — Q waves are fairly deep in leads -aVR,II,aVF,III; and in leads V5,V6 (BLUE arrows in these leads).
• There is loss of r wave between leads V2-to-V3 (RED arrows in these leads).
• This is followed by a deep QS wave in lead V4. There is fragmentation near the beginning of S wave downslope (within the dotted BLUE oval in this lead V4).
• Whereas it is hard to know what to make of the relatively narrow diffuse limb lead Q waves — the chest lead findings of "loss of r wave" + fragmented QS in V4 + much deeper-than-expected Q waves in V5,V6 indicate extensive anterior MI at some point in time.
• Simple pericarditis does not manifest infarction Q waves. But Q waves are common with post-infarction pericarditis.

There is marked and diffuse ST elevation:

• Remarkable for their similarity — 4 successive limb leads ( = leads -aVR,II,aVF,III ) all show Q waves followed by significant J-point ST elevation. Straightening of the ST segments in each of these leads to "my eye" suggests acuity.
• In the face of these 4 successive limb leads showing ST elevation — My "eye" was drawn to mirror-image opposite ST depression in lead aVL and a distinct flattening of the ST segment in neighboring lead I (within the 2 BLUE rectangles).
• ST elevation is marked in leads V3,V4 (more than 4 mm.). Neighboring leads V5,V6 manifest a lesser degree of ST elevation.
• Simple pericarditis does not manifest the kind of reciprocal ST-T wave changes seen in high-lateral leads I,aVL. But the finding of ST elevation in 8/12 leads, in association with the above noted Q waves is probably most consistent with recent extensive infero-antero-lateral MI, now with post-infarction pericarditis.

Final Thoughts:

I wish we knew more about certain specifics regarding today's case. When did the MI begin? When was the VSR? How extensive was this patient's heart disease prior to this recent event?

• The above said — given the patient's age, co-morbidities, and the decision that he was not a surgical candidate, there was little to do clinically that would alter this patient's guarded outcome. 

   

 

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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Magnus (1/13/2025):

Written by Magnus Nossen

The patient in today's case is an 85-year-old man with a history of COPD and dementia. He presented to the emergency department with dyspnea for the past 6 days. He was seen by healthcare providers 4 days prior for shortness of breath and was started on oral antibiotics for suspected pneumonia. He did not improve. Below is his presentation ECG.

What you you think? How do you explain the ST segment elevation in the precordial and limb leads?

The above ECG was originally recorded with a paper speed of 50mm/sec. It has been compressed on the X-axis so that it looks like it was recorded with a paper speed of 25mm/sec. 

My thoughts on the presentation ECG: The ECG shows sinus rhythm at 94 beats per minute. QRS-complexes are narrow, QRS-axis in the frontal plane is close to vertical at 90 degrees. The precordial and inferior leads show ST segment elevation. Let us first look at the precordial leads:

Leads V2 and V3 have miniscule R-waves followed by deep S-waves and ST elevation. Lead V4 has a QS complex followed by ST elevation. There is some R wave in the lateral precordial leads. Leads V3 and V4 both have 6mm ST elevation. The ST to QRS ratio and T-wave to QRS ratio are not compatible with left ventricular aneurysm. The precordial leads show changes consistent with a subacute LAD OMI.

What about the inferior lead ST elevation? Is this ST elevation ischemic in nature? Could the inferior lead ST elevation be due to a “wrap around” LAD that supplies the inferior wall? And if so, could the patient benefit from revascularization?

It would be very strange if the anterior wall shows evidence of completed transmural infarction while the inferior wall myocardium hypothesized to be supplied by the same artery (a "wrap-around" LAD) should be viable. The ST-segments in the inferior leads do not show a typical ischemic looking ST elevation. The ST-segments here are upward concave with distinct J waves in leads II and aVF. There is slight PR-segment depression. This ST-segment elevation morphology is more consistent with pericarditis. 

In summary the ECG is compatible with a subacute completed transmural infarction of the LAD territory. The inferior wall ST-segment elevation is perfectly consistent with that of post infarct pericarditis. This patient will very likely not benefit from revascularization. 

Below is the QoH interpretation with explainability. As you can see, she does not highlight the inferior leads II  and aVF very intensively. Lead V4 which has the highest ST segment to QRS and T wave to QRS ratio is what the AI model notices as most striking. 

A comment on post infarction regional pericarditis: T-wave evolution in patients with post infarct pericarditis is different from T wave evolution in the regular MI patient. Usually T waves will invert within 48 hours. If T waves remain positive beyond 48 hours after MI this ECG finding has a high sensitivity (100%) with a reasonable specificity (77%) for postinfarction pericarditis.  

Patients with suspected ACS should be evaluated with echocardiography. Nowadays pocket sized devices make it possible to quickly get an overview of the heart function of a patient by the bedside. Perhaps not all readers of this blog are experienced seeing echo images. Below I have reproduced a still frame image from the bed side echo done on this patient. The top of the image is closest to the echo probe. The apex of the heart is in closes to the top of the image with the base at the bottom. The heart chamber are annotated. (RA = right atrium. RV = right ventricle. LA = left atrium. LV =left ventricle. IVS = interventricular septum.) 

This video shows the regional wall motion abnormality of the distal septum and apical region of the left ventricle. The distal septum appears thickened. This is not due to hypertrophy. The myocardium appears thickened due to myocardial edema. The edema also makes the necrotic myocardium less echo dense making it appear less "white"

The above echo loop shows a high turbulence flow that traverses the distal interventricular septum. This is consistent with a ventricular septal rupture (VSR). Mechanical complications such as VSR and free wall rupture are associated with post infarct regional pericarditis. This patient as expected presented with a new harsh holosystolic murmur. 

This image show the direction of blood flow from the left ventricle (high pressure system) through the ventricular septal rupture to the right ventricle (low pressure system). If the defect is a large one, pressure across the defect will equalize quickly and the pressure gradient will be low. If the defect on the other hand is small, pressures will not equalize and a pressure gradient can be measured by doppler. The pressure gradient in this case was significant indicating that the defect is rather small. The larger the size of the defect the larger the shunt. Larger shunt volume means less blood exiting the left ventricle through the aortic valve and lower cardiac output.

VSR following myocardial infarction carries a grave prognosis with a virtual 100% one-year mortality without surgical correction. The patient in todays case was not considered a surgical candidate. 

For patients considered candidates for surgery the timing of surgery is crucial. Necrotic myocardium is fragile. Following infarction, metalloproteinase activity and tissue breakdown peak by day 7, whereas deposition of new collagen begins by days 2-4. Necrotic myocytes are entirely replaced by collagen by 28 days and therefore, postponing surgical correction might facilitate successful repair by allowing friable tissue to organize, strengthen, and become well-differentiated from surrounding healthy tissue.

It follows then from the above paragraph that it is important to stabilize patient enough so that surgery can be planned an timed optimally. For more information about the hemodynamic effects and how to manage a patient with VSR see this case.

Learning points: 

• Mechanical complications of transmural infarction are rare and dreaded sequela and have high morbidity and mortality. 
• New onset harsh systolic murmur in a patient with subacute completed MI is VSR or papillary muscle rupture (with acute mitral regurgitation until proven otherwise.
• Post infarction regional pericarditis (PIRP) can be suspected from the ECG and is associated with an increased risk of myocardial rupture.

References:

Wang, S., Liu, H., Yang, P., Wang, Z., & Chen, S. (2024). Current Understanding of Timing of Surgical Repair for Ventricular Septal Rupture following Acute Myocardial Infarction. Cardiology, 1–14. https://doi.org/10.1159/000538967

Vega, J. D. S., Salinas, G. L. A., et. al (2022). Optimal surgical timing after post-infarction ventricular septal rupture. Cardiology Journal, 29(5), 773–781. https://doi.org/10.5603/cj.a2022.0035

Contemporary Management of Post-MI Ventricular Septal Rupture - American College of Cardiology. (2018, July 30). American College of Cardiology. https://www.acc.org/latest-in-cardiology/articles/2018/07/30/06/58/contemporary-management-of-post-mi-ventricular-septal-rupture