Friday, June 22, 2012

ECG Interpretation Review #46 (Inferior - Anterior STEMI - Takotsubo - Stress Cardiomyopathy)


The ECG shown was obtained from a 74-year-old woman who presented with abrupt onset of severe renal colic but no chest pain. Based on findings seen in her ECG — acute cardiac catheterization was performed. Her coronary arteries were normal on cath. Troponins were only minimally elevated. 
  • How would you interpret her ECG? 
  • How might you explain the finding of normal coronary arteries on cardiac catheterization?

Figure 1: ECG obtained from a 74-year old woman with renal colic, but no chest pain.


INTERPRETATION: The ECG shows sinus rhythm at a rate close to 100/minute. The PR and QRS intervals appear to be normal — but the QT is prolonged. The axis is normal (approximately +70 degrees). There is no chamber enlargement. An rSr’ complex is noted in lead V1. 
  • Assessment of Q-R-S-T Changes is remarkable for the presence of inferior Q waves — normal transition (R wave becoming taller than the S wave between leads V3-to-V4) — and ST segment coving with marked elevation in the inferior leads. This is accompanied by deep T wave inversion
  • Similar abnormal ST segment coving and elevation (albeit not as marked) is also present in leads V4,V5. Deep, symmetric T wave inversion that begins in lead V3 is seen in V4,V5. 

Despite the absence of chest pain — the impression from interpretation of this ECG was “probable acute STEMI" (ST-Elevation Myocardial Infarction) with need for immediate cardiac catheterization and probable reperfusion”. Surprisingly, cardiac catheterization revealed normal coronary arteries. Instead — the ventriculogram revealed apical ballooning with hypercontractility of the cardiac base characteristic of Takotsubo Cardiomyopathy. The patient was treated supportively with recovery of left ventricular function over the next few weeks. 
  • Takotsubo Cardiomyopathy is an underappreciated cause of acute ECG abnormalities and new-onset heart failure. The entity was first described in Japan in 1990, with the name takotsubo being derived from a specially designed container used by Japanese fishermen to trap octopuses. The unusual round bottom and narrow neck design of takotsubo resembles the diagnostic picture on cardiac catheterization obtained as a result of ballooning of the cardiac apex with hypercontraction of the base (Figure-2).
  • Other names attributed to this entity include stress cardiomyopathy” and broken-heart syndrome” — in reference to the common occurrence of severe physical or emotional stress prior to onset of the disorder. Awareness of this syndrome is important — because the initial ECG may mimic a large apical infarction (with inferior and anterior ST segment elevation). Transient heart failure is common during the initial stages, but fortunately resolves within a few weeks in most cases.

Figure-2: Collection of actual takotsubo showing the round bottom and narrow neck — that resembles the diagnostic picture seen on the cardiac catheterization ventriculogram (shown here during end-systole). Note characteristic "ballooning of the apex and hypercontractility of the base during cardiac cath (See text).

The Mechanism of Takotsubo CMP (CardioMyoPathy):

The precise mechanism for Takotsubo CMP remains elusive. While factors such as coronary spasm; disturbance of the microcirculation; coronary artery anatomic variation; and neurogenic myocardial stunning have all been implicated — their role is uncertain. What has been shown — is that abnormal response to an increase in endogenous catecholamines is almost always involved. Blood epinephrine and norepinephrine levels are unmistakably elevated (sometimes dramatically) in patients with Takotsubo CMP.

  • In addition — there is more-than-coincidental preceding occurrence of intense situational or psychological stress in many patients. This may be in the form of severe emotional stress (death of a loved one; break-up from significant other; overwhelming anxiety/depression) — painand/or fear (from earthquake or other catastrohic event). It is easy to understand the rationale for other names that have been used for this syndrome (ie, "Stress" Cardiomyopathy or "Broken-Heart" Syndrome).
  • Although consensus is still lacking regarding specific criteria for defining Takotsubo CMP — there is general agreement that cardiac cath is diagnostic (ie, apical ballooning but no "culprit" artery).

 

SUMMARY of the Clinical Picture:

Takotsubo CMP is most typically seen in an older patient (most often in a post-menopausal woman) — who presents with chest pain or new heart failure. Look for the following features:

  • Likelihood of preceding severe physical/emotional stress.
  • Markedly abnormal initial ECG — often with diffuse ST elevation in inferior and antero-lateral leads (apical or LAD "wraparound" distribution). Associated T wave inversion and/or Q waves (sometimes deep) may be seen. Acute extensive STEMI-in-evolution is frequently the initial diagnosis (as it was in today's case).
  • Usually no more than modest troponin elevation (troponins are often elevated — but generally not nearly as high as expected given how marked ECG changes are).
  • Transient LV dysfunction — which may be severe initially (some patients present in pulmonary edema/cardiogenic shock requiring intra-aortic balloon pump support). LV function usually resolves within a few weeks.
  • Possibility of potentially life-threatening arrhythmias during the acute phase (including VT/Torsades de Pointes).
  • Absence of pheochromocytoma, myocarditis or other underlying cardiac pathology to explain findings.
  • Generally favorable prognosis (often with full recovery within 1 month) — but fatalities have been reported (from LV free wall rupture; intractable pulmonary edema).

 

NOTEVariations on the above theme do exist. The syndrome of Takotsubo CMP is not limited to post-menopausal women — the ECG does not always show marked abnormality — and severe stress does not uniformly precede presentation.

  • Anatomic areas other than the apex may also be affected. For example — there may be an “inverted takotsubo” form, in which the apex is spared but the base of the heart is hypokinetic. The existence of such Takotsubo variants helps to explain the likely multifactorial etiology to this interesting syndrome.

 

PEARL: Think of the possibility of Takotsubo CMP when confronted with a patient who presents with a markedly abnormal ECG that doesn’t quite “fit” the clinical picture. 

  • ECG findings may be out of proportion to clinical findings. ECG changes may involve several lead areas (especially inferior and anterior precordial leads — which typically assess the cardiac apex).
  • There may be an element of heart failure. Serum troponins may be positive.
  • The patient is usually an older adult (especially a post-menopausal woman).
  • There has usually been some form of severe preceding “stress”.


============================

ADDENDUM (1/2/2022):

I find it easy to forget about Takotsubo Cardiomyopathy. I've observed that many clinicians have a tendency to overlook this disorder. In the hope of serving as a helpful reminder — I've summarized in Figure-3 below, the ECG Findings that might be expected in Takotsubo Cardiomyopathy (adapted from Namgung in Clin Med Insights Cardiol)


Figure-3: ECG Findings in Takotsubo Cardiomyopathy (adapted from Namgung in Clin Med Insights Cardiol).


============================
Related Material:
  • For another case of Takotsubo Cardiomyopathy — Please see the March 25, 2020 post in Dr. Smith's ECG Blog. Please check out My Comment at the bottom of the page!



Monday, June 11, 2012

ECG Interpretation Review #45 (IVCD - LAHB - Duchenne - Becker - Muscular Dystrophy - LVH - rsr' in V1 -)

The ECG shown was obtained from a 22-year-old man in a wheelchair. 
  • How would you interpret the tracing? 
  • Can you think of a clinical entity that might account for this clinical scenario? 

Figure-1 - 12-lead ECG obtained from a 22-year-old man in a wheelchair. What clinical entity is suggested? 


INTERPRETATION: The ECG shows sinus rhythm at about 70/minute. The PR interval is normal – but the QRS is prolonged to at least 0.12 second. QRS morphology in the 3 key leads (I,V1,V6) is not consistent with either left or right bundle branch block. Therefore — we would classify the conduction defect as nonspecific IVCD (IntraVentricular Conduction Delay)
  • Continuing with the interpretation — We note marked LAD (left axis deviation) consistent with LAHB (Left Anterior HemiBlock). QRS amplitude is markedly increased in lead aVL — although reliability of the ECG diagnosis of LVH (left ventricular hypertrophy) is reduced in the presence of conduction defects.
  • Regarding Q-R-S-T Changes — there are deep and wide Q waves in the high lateral leads (I,aVL). In addition — there is a small q wave in lead V2. 
  • QRS morphology in lead V1 is peculiar, as there is an rSr’s’ complex
  • This is followed by abrupt transition by lead V2, in which a disproportionately tall R wave is noted. 
  • R wave amplitude drops off by lead V3 — with persistent S waves seen throughout the remaining precordial leads. 
  • There is ST segment depression in lateral leads I and aVL which may reflect ‘strain’ from suspected LVH. That said — ST-T wave changes do not appear to be acute. 
-----------------------------------------------
IMPRESSION: This ECG is clearly abnormal and highly unusual for a young adult. Given the history of a “22-year-old man in a wheelchair” should suggest the possibility of a cardiomyopathy such as Duchenne Muscular Dystrophy (DMD). There are over 20 different genetic forms of muscular dystrophy — of which DMD is the most common of these rare disorders. DMD is almost exclusively seen in males, with unfortunate outcome of progressive muscle deterioration and weakness that invariably leads to death at an early age.
  • Cardiac involvement is the rule with most muscular dystrophies. The most common ECG abnormalities in DMD (and in other muscular dystrophies) include the following: i) QRS widening from conduction defects (usually nonspecific IVCD); ii) abnormal Q waves not due to infarction (especially in lateral leads); and iii) a polyphasic rSr’s’ in lead V1 — often with surprisingly tall anterior precordial R waves. All of these features are seen in Figure-1 !
  • Please Click on Figure-2 below for brief review of clinical and ECG features of Duchenne, Becker, and other muscular dystrophies.
-----------------------------------------------
ACKNOWLEDGMENT: My appreciation goes to Dr. Harsha Nagarajarao (of Cardiology Boards) for allowing me to use this tracing.
-----------------------------------------------
Figure-2 - Clinical and ECG features of Muscular Dystrophy.

Friday, June 1, 2012

ECG Interpretation Review #44 (AFib - Flutter - Artifact - Parkinson - Tremor)

The lead II rhythm strip shown in Figure 1 was observed on telemetry. 
  • Is the patient in atrial flutter?

Figure 1 – Lead II rhythm strip observed on telemetry. Is this atrial flutter?


INTERPRETATION: At first glance — one might be tempted to say atrial flutter was present. However, more careful inspection suggests that the baseline deflections do not represent atrial activity at all. In adults — atrial activity with atrial flutter is almost always regular at a rate of between 250-to-350/minute. Typically it manifests a “sawtooth” pattern in lead II. The deflections in question for this example are more geometric in configuration (ie, vertical) – they are irregular — and they far exceed the expected rate range for atrial flutter in an adult because they occur at a rate of between 400-to-500/minute. A look at the patient confirmed that these small amplitude vertical deflections were the result of tremor artifact
  • It is difficult to determine what the true rhythm in Figure 1 really is. The rate (95-to-100/minute), apparently normal QRS duration, and near regularity of the rhythm suggest a sinus etiology. 
  • That said – from this tracing alone, one could not rule out the possibility of either accelerated junctional rhythm (since no definite P waves are seen) — or atrial fibrillation (since there is a slight irregularity to the rhythm). 
  • IF there was a need to know clinically — one could either attempt to repeat the rhythm strip or obtain a 12-lead ECG in the hope that other leads might be less distorted by artifact. 
------------------------------------------------------- 
About ARTIFACT: Although admittedly devious on our part to show artifact in our Blog – we intentionally do so because: 
  • Artifact is an extremely common finding in the real world. 
  • Patients have been medicated, and even cardioverted or defibrillated when artifact has not been recognized or has been misinterpreted. 
  • Familiarity with the common types of artifact encountered, and attention to a few basic points usually makes recognition easy. 
  • Failure to actively include the possibility of artifact into your differential greatly increases the chance of it being overlooked. 
BOTTOM LINE: Suspect artifact whenever physical or electrocardiographic findings do not “fit” with the arrhythmia diagnosis being contemplated. Thus, a chaotic pattern without any organized activity cannot be ventricular fibrillation if the patient remains awake and alert. Similarly, deflections occurring at a rate of 400-to-500 times/minute (as shown in Figure 1) are far too rapid to be atrial flutter — especially in view of the morphology, irregularity, and clinical history (of tremor) in this case. 
  • PEARL: Parkinsonian tremor typically occurs at a speed of 4-to-6 cycles per second. This is close to the speed of atrial flutter — so the two entities may easily be confused. KEY distinguishing features of Parkinsonian tremor are: i) irregularity of tremor deflections; ii) more geometric appearance (up-and-down) than “sawtooth”; and, iii) the patient will manifest tremor … 
----------------------------------------------------