Why the sudden shock after a few days of malaise?

Written by Magnus Nossen - Edits by Grauer and Smith

The patient in today’s case is a woman in her 70s with a previous medical history of HTN and hyperlipidemia. She presented to an outside hospital after several days of malaise and feeling unwell. At the time of admission, her vital signs were normal. Heart rate was in the 80s. She had a very elevated troponin T at 12,335 ng/L at the time of presentation. (This is a value typical for a large subacute MI, normal value < 0-14ng/L.)  

Below is the presentation ECG.

The patient initially denied chest pain, but when questioned directly — did admit to vague "chest discomfort" in previous days. She was transferred to our facility for angiography. On arrival she was without distress. Due to acute renal failure and the duration of her symptoms over a number of days — it was decided to perform angiography the following day. Serial Troponin T values were decreasing, consistent with subacute completed MI. The ECG on admission showed sinus rhythm with a heart rate in the 80s — and was consistent with a subacute completed inferior, lateral and posterior transmural infarction, with Q waves and ST elevation in the inferiolateral leads — and ST depression in lead V2. The patient was put on telemetry while waiting for angiography the following day.

The patient awoke suddenly during the night — stating that she felt "strange". The ECG below was recorded at this time. What do you think?

This ECG is consistent with infero-postero-lateral infarction — with persistent inferior lead ST elevation and reciprocal high-lateral ST depression — ST depression in lead V2 — and some terminal T wave inversion in inferior and lateral chest leads. It is not significantly different from the admission ECG. Perhaps the most remarkable change — is the increase in heart rate, with this ECG now showing sinus tachycardia at 118/minute! Also of note is the still upright (not inverted) T waves. Persistent ST elevation with upright T waves >48 hours after myocardial infarction is associated with Post-Infarction Regional Pericarditis (PIRP).

Sinus tachycardia has many potential causes. In my experience, for the patient at rest and not anxious — it often signifies severe illness. This is especially true for the elderly patient with sinus tachycardia. The patient in today’s case suddenly became tachycardic while sleeping. The heart rate almost doubled within a minute. What might account for the sudden rate change in this patient? See if you can identify the problem in the below parasternal view of the heart.

The above video file was recorded from a subcostal «window» and it shows the heart with all four chambers. Right atrium, right ventricle, left atrium and left ventricle viewed through the liver. What is the cause of the sudden tachycardia? 

Below is a still image from the above video. The heart chambers are annotated. From the subcostal "window" the heart is viewed through the liver and thus the liver parenchyma is closest to the transducer (top of the image). Below the liver is the heart with the right atrium (RA), right ventricle (RV), left atrium (LA) and left ventricle (LV) The red arrow points to a large opening in the basal region of the interventricular septum. This is a ventricular septal rupture (VSR). As already mentioned, this patient could have post-infarction regional pericarditis from a large completed MI. PIRP is strongly associated with myocardial rupture. This patient developed a rupture of the basal portion of the interventricular septum (VSR). The VSR is what is causing the cardiogenic shock!

A Short Comment on PIRP and T Waves: 

Oliva et al found a strong association of myocardial rupture with postinfarction regional pericarditis. PIRP was associated with persistent upright T waves. He found two types of atypical T wave development in PRIP

1) Persistently positive (upright) T waves beyond 48 hours in a patient with acute MI

2) Premature change from inverted T waves to pseudonormal T waves (within 48-72 hours) 

In our case, PIRP is a likely explanation for the continued positive T waves. Since serial ECGs are not available so either of the two patterns described above could be present (only serial ECG could differentiate). 

Another possible cause of pseudonormalization of T waves mentioned many times on this blog is the pseudonormalization caused by re-occlusion of an infarct related reperfused coronary artery. This does not fit with the clinical scenario in today's case. 

Below are two more video files. These images were obtained  from the parasternal short axis which transects the left and right ventricles. The VSR is located in inferior and basal portion of the ventricular septum and is readily visible. The second video file below shows the shunt by color doppler. 

Discussion: The patient in today’s case experienced a mechanical complication secondary to completed OMI. Troponin at presentation was very significantly elevated and T waves were still upright. She had atypical symptoms which made her postpone seeking medical attention. Mechanical complications secondary to myocardial infarction are infrequent due to most patients receiving revascularization quite rapidly. The patient in today’s case developed a large basal septal ventricular septal rupture (VSR) as a complication of an untreated OMI. Auscultation of a NEW harsh holosystolic murmur lead to rapid evaluation with echocardiography that confirmed the clinical suspicion. 

A VSR will lead to sudden left to right shunt and if large enough can lead to low output left sided failure. The RV acts as a conduit and does not necessarily become acutely dilated. Left ventricular afterload reduction is essential to decrease the trans-septal pressure gradient and thus decrease shunt volume, making a larger proportion of the blood flow from the left ventricle through the aortic valve.

For the patient in today's case nitroprusside (vasodilator) infusion was started to lower systemic vascular resistance (SVR), and an intra aortic balloon pump (IABP) was placed to further decrease afterload and better the hemodynamics. Surgical repair of the VSR was eventually done. The patient needed short term dialysis post surgery, but she eventually made a full recovery.

Mechanical complications are dreaded sequela of myocardia infarctions and can  come in the form of free wall rupture, ventricular septal rupture or papillary muscle rupture. The true incidence of the three mechanical complications may differ from reported incidence due to underreporting, miscoding, or variation in the populations studied. It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. Among patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common. 

Mechanical complications occur acutely and significantly alter hemodynamics leading to compensatory mechanism which usually involve vasoconstriction and tachycardia, both hallmarks of cardiogenic shock. 

A VSR is more likely to occur in patients who are older, female, hypertensive, have chronic kidney disease, and have no prior history of smoking. It commonly occurs in the setting of a first myocardial infarction (MI) in the background of delayed or absent reperfusion therapy. Angiography usually reveals an absence of collateral circulation to the infarct zone. 

Because previous ischemia induces myocardial preconditioning, decreasing the likelihood of transmural myocardial necrosis and myocardial rupture, patients with evidence of diabetes mellitus, chronic angina or previous MI are less likely to experience a rupture. VSR may develop within 1-14 days post MI, however it’s incidence usually shows a bimodal peak which is within 24 hours and after 3-5  days post MI.

Survival after ventricular septal rupture may occur only after surgical repair. Thus, the diagnosis of ventricular septal rupture should prompt a heart team discussion of options. This discussion should take into account that, for some patients, surgery is futile as mortality approaches 100 percent. Older patients and those with poor right ventricular function often fall into this group. The timing of ventricular septal rupture repair is controversial.

Subacute AnteroSeptal STEMI, With Persistent ST elevation and Upright T-waves

Learning Points:

1. Sinus tachycardia (especially in the elderly) often signifies serious illness as it did in today’s case.
2. Mechanical complications of transmural infarction are rare and dreaded sequela and have high morbidity and mortality. 
3. Post infarction regional pericarditis (PIRP) can be suspected from the ECG and is associated with an increased risk of myocardial rupture.

Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis

Oliva PB.  Hammill SC.  Edwards WD.  Cardiac rupture: a clinically predictable complication of acute myocardial infarction

Ventricular septal rupture

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MY Comment, by KEN GRAUER, MD (9/5/2024):

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As I emphasized in My Comment in the December 6, 2022 post and the August 19, 2023 post of Dr. Smith's ECG Blog — Not all patients with acute MI report chest pain. I thought the presentation of today's case makes it worthwhile to review the data regarding this issue.

• As per Dr. Nossen — today's patient concerns an older woman with a several day history of malaise and "not feeling well". Mention of vague "chest discomfort" over a period of recent days was only elicited when specifically requestioned. By history — providers were not expecting her initial ECG to show recent completed infarction with marked Troponin elevation.

The Framingham studies from many years ago taught us that the incidence of “Silent MI” is as high as ~30% of all MIs (Kannel & Abbott: N Engl J Med 311(18):1144-1147, 1984 — Kannel: Cardiol Clin 4(4):583-591, 1986).

• The interesting part of this data is that in about half of this 30% (ie, ~15% of all patients with MI) — patients found on yearly follow-up ECGs to manifest clear evidence of infarction had NO symptoms at all — therefore truly “silent” MIs.
• But in the other half of this 30% (ie, in ~15% of all patients with MI) — although these patients found on follow-up ECG to have had infarction did not have chest pain — they did have "something else" thought to be associated with their MI.
• The most common “something else” symptom was shortness of breath. Other non-chest-pain equivalent symptoms included — abdominal pain — “flu-like” symptoms (ie, myalgias; not “feeling” good) — excessive fatigue — syncope — mental status changes (ie, as might be found in an elderly patient wandering from home).
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• BOTTOM Line: It's especially important for emergency providers to be aware of the entity of “Silent MI” — which can either be completely “silent” — or, associated with a non-chest-pain equivalent symptom. The incidence of both types of silent MI is more common than is often appreciated. Not all patients with acute (or recent) MI have chest pain with their event.

Application to Today's Case: Today's patient developed ventricular septal rupture the evening after she was admitted to the hospital. Her nonspecific symptoms that brought her to the hospital began a number of days before she finally sought medical assistance. 

• Awareness that this patient's malaise and her "not feeling well", as well as her vague chest discomfort might represent a cardiac problem — could have resulted in more timely initiation of treatment, that potentially might have averted the severe mechanical complication of her initially unrecognized extensive infarction.