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How is the diagnosis differentiated?
Medication tips
Today I would like to report three interesting cases: patients have chest tightness, with or without heart failure, ECG has ST-segment elevation, and coronary angiography + left ventricular angiography has been performed, but the final diagnosis is not myocardial infarction.
Case 1
Case introduction
The patient, a 75-year-old woman, was admitted to the hospital for "chest tightness for 5 days" and had a history of hypertension for more than ten years.
Check the results
There were no obvious abnormalities in the heart and lungs for admission.
ECG illustration II III aVF V2-6 ST segment arched back up, elevation 0.1 mv, coronal T wave inversion, QTC prolongation, 549ms.
Creatine kinase isoenzyme quantification is 15.040 ng/ml, troponin I is quantified 3.220 ng/ml, and myoglobin is normal.
Acute ST-segment elevation myocardial infarction is considered, and coronary angiography suggests no stenosis of blood vessels. Left ventricular contrast shows a marked weakening of apical activity and spherical bulging during systolic phase.
Ask for medical history
Asked for medical history, the patient had a history of emotional agitation about 1 week ago, and then developed chest tightness.
Fixed diagnostics
Stress cardiomyopathy. Drug treatment with metoprolol, benazepril and other drugs. After that, the patient's symptoms gradually resolve. Follow-up follow-up to review the heart ultrasound, ECG returned to normal.
Fig. 1 Left: The patient's ECG is widely elevated in the ST segment with coronary T waves, and QTc is significantly prolonged. Right: Left ventricular angiography shows an octopus basket-like systolic phase, decreased apical beats, and normal or compensatory contraction of the basal segment.
analyse
The patient has ST segment elevation, elevated troponin, and chest tightness, resembling myocardial infarction. But the first ECG has revealed a difference from conventional myocardial infarction — a general ST-segment elevation rather than a segmental one.
Eventually, left ventricular angiography was diagnosed as stress cardiomyopathy. Note that diagnosis requires exclusion of adrenal medullary tumors.
Case 2
The patient, a 52-year-old man, was admitted to the hospital for "repeated chest tightness and discomfort for half a year" and was previously in good health.
Examination of the apex of the heart and systolic murmurs, no significant abnormalities remain.
ECG diagram: Chest lead ST segment arched upwards, with T wave inversion.
Cardiac ultrasound: left ventricular end-diastolic end-inner diameter 46 mm, left ventricular function measurement: ejection fraction (EF) 66%, apical extrusion outward, range of about 28 mm * 24 mm, ventricular septum 15.2 mm.
At that time, we considered the ECG as the evolution of myocardial infarction, and diagnosed old myocardial infarction and the formation of ventricular wall tumors.
Coronary angiography suggests: 20% to 30% stenosis of the caudal plaque of the left coronary trunk (LM), mild plaque of the near middle segment of the left anterior descending branch (LAD), unsmooth intima of the left gyrospinar branch (LCX) without significant stenosis, and 40% to 50% of the proximal plaque stenosis of the right coronary artery (RCA). There is no severe stenosis of the coronary veins.
Left ventricular angiography shows obstruction in the middle of the left ventricle, the catheter fails to reach the apex, and the apical movement is weakened.
Hypertrophic central left ventricular obstructive cardiomyopathy.
Figure 2 Left: ECG chest lead ST segment arched upwards with T wave inversion. Right: left ventricular contrast shows dumbbell-shaped systolic phase, central obstruction, apical ventricular wall tumor formation.
Left ventricular central obstructive cardiomyopathy is a rare subtype of hypertrophic cardiomyopathy. Myocardial hypertrophy is located in the middle of the ventricular septum and left ventricle, often accompanied by the formation of apical ventricular wall tumors. The pressure level difference is located at the basal and apex of the heart, rather than the traditional left ventricular outflow tract. Obstructive cardiomyopathy in the middle of the left ventricle may be heard at the apex of the heart and is weaker than systolic murmur. ECG may show elevation of the ST segment of the chest lead. There is no specific treatment for this disease.
Obstructive cardiomyopathy in the middle of the left ventricle is relatively rare, and I have only seen it in books before. Regarding the "pressure scale difference is located at the base and apex, not in the left ventricular outflow tract", I have always had doubts before, but now I feel that I understand. In this regard, all teachers are welcome to discuss and exchange ideas in the comment area.
Case three
The patient is a female, 79 years old. He was admitted to the hospital for "repeated chest tightness and shortness of breath for more than 3 years, and then another 3 days of companionship".
The general condition of the examination is weak, the atrial fibrillation of the auscultation of the heart, and the murmur is not reached.
ECG shows atrial fibrillation, II III aVF V4-6 ST segment elevation 0.1-0.3 mv.
Cardiac ultrasound: left ventricular end-diastolic end inner diameter 37 mm, ventricular septum and apex thickening, ventricular septum intermediate segment thickness of about 17 mm, left ventricular EF 30%, left ventricular wall segments of the general weakening of movement.
Patients have chest tightness, ST segment elevation, and myocardial infarction cannot be ruled out.
Coronary angiography: no significant stenosis in LM, mild plaque in the near-midparts of LAD, mild plaques in the mid-LCX segment, and mild plaques in the distal RCA segment. Coronary artery lesions do not explain the condition.
Left ventricular contrast shows that the left ventricular apex and the middle of the ventricular septum are significantly hypertrophied, and the PIG catheter cannot reach the apex.
Apical hypertrophic cardiomyopathy? Cardiac insufficiency.
Figure 3 Left: ECG shows atrial fibrillation with II III aVF V4-6 ST segment elevation 0.1-0.3 mv. Right: Left ventricular angiography shows hypertrophy of the apex of the heart and "spades" during systolic phase.
This patient is a chronic course, the ECG has ST-segment elevation, and the cardiac ultrasound shows a significant decrease in cardiac function. However, there are no serious lesions in the coronary veins. Left ventricular contrast suggests hypertrophy of the apex of the heart and a spade-shaped systolic phase.
For this patient's apex hypertrophic cardiomyopathy, the author put a question mark. Because I think she is probably not fat.
Most of the patients with apex hypertrophic cardiomyopathy that I have seen before have no clinical symptoms, and they are further treated after the ecG abnormality is found on physical examination, and the cardiac contractility function is mostly normal.
This patient has very poor heart function, and the author thinks that she is more likely to have invasive or storage cardiomyopathy, and at that time suggested that she go to a higher hospital for cardiac MRI or endocardial biopsy. Unfortunately, the patient did not go, and finally the heart failure became more and more serious, and the prognosis was poor.
summary
The author introduced 3 interesting cases here, the patient's symptoms and ECG have the same, all did coronary angiography + left ventricular angiography, and ultimately did not consider coronary heart disease, the results are also very different.
Perhaps you can provide ideas for the identification of chest pain in the future, especially in the last case, the diagnosis is still in doubt, welcome to have an idea of teachers or friends can discuss with the author in the comment area.
Source of this article: Cardiovascular Channel of the Medical Community
This article is written by Aaron
Editor-in-Charge: Yuan Xueqing, Zhang Li
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