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some board questions about cardiology (转载)请教,买神末样的听诊器
求教:妈妈冠心病的治疗选择(附CT图)CK form 1 block 2 Q18 help needed
冠心病的检查的方法及危险【intern 日记】终于熬过第一周了
心律不齐的问题南山,看看这个
求助:脑血栓!!! (转载)********MedicalPractice SuperBowl 现在开始**************
几篇期刊文章请心血管医生帮分析,谢谢!
Inquiry about the calcium supplement for kindney malfunction patients怄气,然后心脏轻微疼痛,什么问题
Heart Disease and Stroke Statistics—2013 Updatesome board questions about cardiology
相关话题的讨论汇总
话题: st话题: segment话题: patient话题: elevation话题: coronary
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1 (共1页)
f******w
发帖数: 10267
1
活动宗旨:分享学习提高
开始日期:即日
截至日期:11/30/2011
内容要求:真实案例,图文并茂。文章200字以上,附图不限。每一篇参赛的必须是一
个独立完整的故事。请参加活动的同学在题目上注明[参加活动]。
奖励方式:每篇参赛文章均得100伪币。
f******w
发帖数: 10267
2
活动宗旨:分享学习提高
开始日期:即日
截至日期:11/30/2011
内容要求:真实案例,图文并茂。文章200字以上,附图不限。每一篇参赛的必须是一
个独立完整的故事。请参加活动的同学在题目上注明[参加活动]。
奖励方式:每篇参赛文章均得100伪币。
a*********1
发帖数: 872
3
本次活动到月底就结束了,期待更多的人来参与,机不可失,时不再来!
g*2
发帖数: 658
4
刚看到有趣病例活动,想到 broken heart syndrome。 在我短短的几个月住院第一年
中,居然看到了2例。 一例是copd induced, 例外一例可能是GBS induced.
basically broken heart syndrome is transient stress induced cardiomyopathy,
aka Takotsubo cardiomyopathy/apical ballooning syndrome
a sudden onset of congestive heart failure associated with ECG changes
suggestive of an anterior wall myocardial infarction. in my 1st case, pt's
ECHO when admitted showed basal segment thickening w/ remaining hypokinetic
ventricle walls, severely decreased LV systolic function with EF 20-25%. 11
days later, rpt echo showed EF 60-65% with LV systolic function nml and no
wall abnomality. Trop decreased from 0.68 to 0.06, pro-BNP dropped from 13 k
to 5 k.

【在 a*********1 的大作中提到】
: 本次活动到月底就结束了,期待更多的人来参与,机不可失,时不再来!
A*******s
发帖数: 9638
5
What is the underlying mechanism? Overwhelming adrenaline surge?
我想这个broken heart 跟我们平时讲的伤心应该有所不同吧? 我们说的伤心应该跟
low serotonin有关。 :)

,
hypokinetic
11
k

【在 g*2 的大作中提到】
: 刚看到有趣病例活动,想到 broken heart syndrome。 在我短短的几个月住院第一年
: 中,居然看到了2例。 一例是copd induced, 例外一例可能是GBS induced.
: basically broken heart syndrome is transient stress induced cardiomyopathy,
: aka Takotsubo cardiomyopathy/apical ballooning syndrome
: a sudden onset of congestive heart failure associated with ECG changes
: suggestive of an anterior wall myocardial infarction. in my 1st case, pt's
: ECHO when admitted showed basal segment thickening w/ remaining hypokinetic
: ventricle walls, severely decreased LV systolic function with EF 20-25%. 11
: days later, rpt echo showed EF 60-65% with LV systolic function nml and no
: wall abnomality. Trop decreased from 0.68 to 0.06, pro-BNP dropped from 13 k

g*2
发帖数: 658
6
broken heart 和 depression 应该不同吧。其实pathogenesis还是不清楚。
hypotheses include catecholamine excess, coronary artery vasospasm,
microvascular dysfunction leading to temporary stunning of myocardium,
possible direct catecholamine myocardial toxicity.

【在 A*******s 的大作中提到】
: What is the underlying mechanism? Overwhelming adrenaline surge?
: 我想这个broken heart 跟我们平时讲的伤心应该有所不同吧? 我们说的伤心应该跟
: low serotonin有关。 :)
:
: ,
: hypokinetic
: 11
: k

A*******s
发帖数: 9638
7
Just kidding. Broken heart and heartbroken are different, aren't they? :)

【在 g*2 的大作中提到】
: broken heart 和 depression 应该不同吧。其实pathogenesis还是不清楚。
: hypotheses include catecholamine excess, coronary artery vasospasm,
: microvascular dysfunction leading to temporary stunning of myocardium,
: possible direct catecholamine myocardial toxicity.

g*2
发帖数: 658
8
good q. wiki - A broken heart (or heartbreak) is a common metaphor used to
describe the intense emotional pain or suffering one feels after losing a
loved one, whether through death, divorce, breakup, physical separation or
romantic rejection.

【在 A*******s 的大作中提到】
: Just kidding. Broken heart and heartbroken are different, aren't they? :)
g*2
发帖数: 658
9
刚刚把堆积了几个星期的nejm翻看了一下,居然在11月底的那期case discussion就是
讲得这个病
http://www.nejm.org/doi/full/10.1056/NEJMcpc1103565
Case 36-2011 — A 93-Year-Old Woman with Shortness of Breath and Chest Pain
Presentation of Case
Dr. Pooja Agrawal (Emergency Medicine): A 93-year-old woman was seen in the
emergency department at this hospital because of chest pain and shortness of
breath.
The patient had been in her usual state of health, with hypertension and
chronic renal insufficiency, until the morning of admission, when she was
awakened by stabbing substernal chest pain that radiated to the left
shoulder and jaw and was associated with shortness of breath. She called
emergency medical services; on evaluation, an electrocardiogram reportedly
showed ST-segment elevations. Acetylsalicylic acid was administered orally,
and nitroglycerin was given sublingually (three doses). She was brought to
the emergency department of this hospital, arriving 3 hours after the onset
of chest pain.
The patient rated the pain at 7 on a scale of 1 to 10 (with 10 indicating
the most severe pain). She had a history of hypertension, renal-artery
stenosis (for which a stent had been placed 2.5 years earlier), chronic
renal insufficiency, gastroesophageal reflux disease, hypercholesterolemia,
cholelithiasis, osteoporosis, osteoarthritis, and dementia involving poor
memory and insight. Adenocarcinoma of the colon 4 years earlier had been
treated with a sigmoid colectomy; recovery was complicated by a
postoperative myocardial infarction. The patient had had a hysterectomy and
cataract surgery in the past. Medications included clopidogrel, amlodipine,
atorvastatin, omeprazole, labetalol, clonidine, and acetylsalicylic acid.
She was allergic to sulfa drugs; hydrochlorothiazide had caused hyponatremia
, and irbesartan had caused kidney dysfunction. She was a widow; she lived
with a friend and had assistance in the home from elder services. She did
not smoke, drink alcohol, or use illicit drugs. Her sister had hypertension,
atrial fibrillation, and adenomatous colonic polyps; other relatives had
had congestive heart failure.
On examination, the patient appeared alert and frail; she was oriented to
person and season but not to date or day. The temperature was normal, the
blood pressure 199/108 mm Hg, the pulse 116 beats per minute and regular,
the respiratory rate 18 breaths per minute, and the oxygen saturation 98%
while she was breathing ambient air. The height was 147.3 cm, and the weight
44.6 kg. The heart sounds were rapid, with a regular rhythm and no murmurs,
and there was trace ankle edema bilaterally. The remainder of the
examination was normal. The level of creatine kinase MB isoenzymes was 10.9
ng per milliliter (reference range, 0.0 to 6.9), creatine kinase 89 U per
liter (reference range, 40 to 150), creatine kinase isoenzymes index 12.2% (
reference range, 0.0 to 3.5) and troponin T 0.40 ng per milliliter (
reference range, 0.00 to 0.09). Results of other laboratory tests were
normal, including complete blood count; plasma levels of electrolytes,
calcium, phosphorus, and magnesium; and tests of renal function and
coagulation. An electrocardiogram showed sinus tachycardia at 119 beats per
minute, with ST-segment elevations up to 3 mm in leads V1, V2, and V3 (most
prominent in V2) with more subtle ST-segment elevation in leads I and aVL. Q
waves were present in leads V2 and V3. A chest radiograph showed low lung
volumes, with right basilar subsegmental atelectasis, which was unchanged as
compared with a study 11 months earlier. Heparin, eptifibatide, and
metoprolol were administered intravenously within 5 minutes after arrival.
A diagnostic procedure was performed.
Differential Diagnosis
Dr. Emily L. Senecal: I am aware of the diagnosis in this case. This patient
presented to the emergency department with chest pain and shortness of
breath. When a patient such as this one, with chest pain or an anginal
equivalent, arrives in the emergency department, the standard of care
according to the joint guidelines of the American College of Cardiology and
the American Heart Association is that an electrocardiogram (ECG) should be
obtained within 10 minutes after the patient's arrival.1 The goal is to
assess for evidence of myocardial infarction with ST-segment elevation. This
patient's ECG showed ST-segment elevation. However, conditions that mimic
myocardial infarction with ST-segment elevation should be considered.
Aortic Dissection
It is crucial to consider the diagnosis of aortic dissection in this patient
who presented with chest pain and ST-segment elevation on ECG, because the
treatments for acute coronary syndrome and aortic dissection differ. Aortic
dissection can cause myocardial infarction with ST-segment elevation when
the dissection propagates proximally to involve a coronary artery, most
commonly the right coronary artery. The mechanism by which ST-segment
elevation occurs is incompletely understood, but it may result from
obstruction of the ostium of the right coronary artery by the intimal flap
or from extension of the dissection into the right coronary artery itself,
with associated luminal compression by the dissecting hematoma.2 An
international registry of 464 patients with aortic dissection showed that 4.
8% of the 256 patients with dissections involving the ascending aorta had
new ST-segment changes or Q waves that were consistent with acute myocardial
infarction.3
In this case, the patient's history of hypertension increased her risk for
aortic dissection; however, her clinical presentation was not typical for
dissection. Her pain worsened over the next several hours, was not
accompanied by back pain, and was not described as stabbing, tearing, or
ripping. Also, her mediastinal silhouette was not widened on chest
radiographs.
Acute Pericarditis
Acute pericarditis should be considered in the differential diagnosis of
this patient, because standard anticoagulation treatments for acute coronary
syndrome may cause hemorrhagic pericardial effusion and cardiac tamponade
in patients with acute pericarditis. The classic ECG findings early in the
course of acute pericarditis are ST-segment elevation in all leads except
aVR and V1, in which there is reciprocal ST-segment depression. PR-segment
depression typically accompanies ST-segment elevation on ECG in this early
stage (stage I). As the disease progresses, the ST and PR segments normalize
(stage II), followed by T-wave inversion (stage III) and then normalization
of the T waves (stage IV).
Unlike the findings in this patient and in acute coronary syndrome, in which
ST-segment elevation is focal and corresponds to the occluded coronary
artery, ST-segment elevation in acute pericarditis is diffuse because the
entire pericardium is involved. Focal pericardial inflammation is uncommon
but, when present, results in ST-segment elevation in isolated leads that
may confound the diagnosis. Another distinguishing factor in acute
pericarditis is the morphologic features of the ST segments; in acute
coronary syndrome, the ST segments are typically convex (dome-shaped),
whereas in acute pericarditis, they are typically concave up (cup-shaped).
In this patient, neither the clinical presentation nor the ECG was typical
of acute pericarditis.
Pulmonary Embolism
Could this patient have a pulmonary embolism? The most common
electrocardiographic findings in patients with acute pulmonary embolism are
sinus tachycardia, complete or incomplete right bundle-branch block, ST-
segment depression or T-wave inversion in the precordial leads, and the
S1Q3T3 pattern (prominence of the S wave in lead I and a Q-wave and T-wave
inversion in lead III). However, there are case reports of massive pulmonary
embolism presenting with ST-segment elevation in the precordial leads.4
Although this patient did not have any known risk factors for pulmonary
embolism, she did have chest pain and shortness of breath, tachycardia on
arrival in the emergency department, and ST-segment elevation in the
precordial leads on ECG. Thus, acute pulmonary embolism remains a
consideration.
Myocarditis
The clinical presentation of myocarditis varies from subclinical fatigue to
sudden, unexplained death. Chest pain may be the presenting symptom, and
symptoms of heart failure are common. A preceding viral illness is classic
but not universal. Patients with acute myocarditis may have normal ECG
findings or may have a wide range of abnormalities, including ST-segment
elevation that mimics acute coronary syndrome. In a study of 45 patients
with presumed acute coronary syndrome but with normal findings on coronary
angiography, a diagnosis of myocarditis was made in 35 (78%).5 This patient
did not report a preceding illness or have signs of heart failure, but the
variability in the presentation of myocarditis necessitates keeping this
condition in the differential diagnosis.
Left Ventricular Aneurysm
This patient had had a myocardial infarction 4 years earlier. Left
ventricular aneurysm most commonly occurs after a large myocardial
infarction of the anterior wall, although it may result from an inferior-
wall myocardial infarction. Approximately 50% of left ventricular aneurysms
develop within 2 days after an acute myocardial infarction, and the other 50
% within 2 weeks after an infarction.6 The increased diameter of the left
ventricular cavity caused by a left ventricular aneurysm leads to increased
wall stress and oxygen demand,7 with ECG findings of persistent ST-segment
elevation and Q waves in the precordial leads. Such findings were seen on
this patient's presenting ECG but not on her baseline ECG from 8 months
previously. Thus, a left ventricular aneurysm is unlikely.
Early Repolarization
Early repolarization is a common cause of ST-segment elevation and should be
considered in all patients presenting to the emergency department with
chest pain and ST-segment elevation on ECG. Early repolarization is seen on
ECG in 1 to 5% of the general population8 and in up to 48% of patients
presenting to the emergency department with chest pain.9 One study of 93
patients treated with thrombolytic agents for presumed acute myocardial
infarction showed that 10 (11%) of the patients did not actually have an
infarction; 3 of these 10 patients had early repolarization.10 ECG findings
in cases of early repolarization include diffuse ST-segment elevation (most
often in the precordial leads), concave upsloping of the initial part of the
ST segments, notching of the J point, and T waves that are symmetric and
concordant and have a large amplitude.9
Early repolarization is more common in men, patients who are younger than 40
years of age, blacks, and patients who are physically active.11 Those
descriptors do not apply to this patient.
Prinzmetal's Angina
Prinzmetal's angina, also known as variant angina, results from transient
coronary vasospasm. The presence of ST-segment elevation that resolves when
symptoms abate establishes the diagnosis. Patients with Prinzmetal's angina
typically are younger than this patient and do not have the classic risk
factors (other than cigarette smoking) for acute coronary syndrome.
In summary, this patient presented with acute chest pain and ST-segment
elevation in the precordial leads that was not seen on her baseline ECG. Our
clinical diagnosis was myocardial infarction with ST-segment elevation.
The patient was sent to the cardiac catheterization laboratory.
Dr. Emily L. Senecal's Diagnosis
Acute myocardial infarction with ST-segment elevation.
Diagnostic Testing
Dr. Kenneth Rosenfield: The patient was met by the members of the
interventional cardiology team, who had been notified of her impending
arrival while she was in transit to the hospital. Evidence shows that early
restoration of myocardial blood flow leads to a dramatic reduction in
mortality among patients with myocardial infarction with ST-segment
elevation.12,13 As a result, rapid mechanical reperfusion with balloon
angioplasty and stenting has became the standard of care.14,15 Thus, the
phrases “time is muscle” and “door-to-balloon time” (the interval from
the patient's arrival at the emergency department to restoration of flow)
have become part of our daily vernacular.
The beneficial effect of early reperfusion has led to a change in the
systems of care delivery that mandates close coordination between the
emergency department and the catheterization laboratory. This case is
representative of the current approach to patients with suspected acute
coronary syndromes — when this patient arrived with chest pain, the
emergency department staff was expected to obtain and interpret the ECG
within 10 minutes and determine whether she was having a myocardial
infarction with ST-segment elevation. As is now routine throughout the
United States, accurate and expeditious diagnosis of myocardial infarction
with ST-segment elevation is the responsibility of the emergency department
physician, who is responsible for deciding whether to activate the cardiac
catheterization laboratory for urgent angiography. This represents a
dramatic shift in process and culture.
Interventional cardiologists have also had to adjust. As occurred in this
case, interventional cardiologists now routinely arrive at the
catheterization laboratory simultaneously with the patient. They must
rapidly evaluate and decide whether to proceed with an intervention.
Fortunately, the collaborative efforts of emergency department staff and
cardiologists to reduce door-to-balloon time has actually led to reduced
mortality.15 However, the initiative of door-to-balloon time carries with it
a certain risk. Some triaged patients who actually do not have acute
coronary occlusion may be moved urgently to the catheterization laboratory.
For some of these patients, angiography is not recommended, and we hope that
the cardiologist recognizes that before proceeding. In other patients, such
as this one, urgent catheterization is indicated to rule out the diagnosis
of coronary occlusion with associated myocardial infarction and ST-segment
elevation.
Coronary Angiography and Left Heart Catheterization
Dr. Angel E. Caldera: After we obtained written informed consent from the
patient, access was obtained through the right common femoral artery.
Diagnostic coronary angiography was performed, with contrast material
injected by means of standard diagnostic catheters.
Left coronary angiography revealed a normal left main artery that gave rise
to a long left anterior descending artery (with several diagonal branches)
and a small, nondominant left circumflex artery. The diameter of the middle
portion of the left anterior descending artery tapered at the level of the
bifurcation with the third diagonal branch but showed minimal stenosis. The
remainder of the left anterior descending artery, the diagonal branches, and
the left circumflex artery had no substantial stenosis (Figure 1AFigure
1Cardiac Catheterization.). Right coronary angiography revealed a dominant
right coronary artery from which the posterior descending artery and two
posterolateral branches originated. The right coronary artery and its
branches were free of clinically significant disease (Figure 1B).
An angled pigtail catheter was advanced across the aortic valve into the
left ventricle. Left ventriculography was performed in the right anterior
oblique projection, with power injection of contrast material. This revealed
akinesis of the anterior wall, hypokinesis of the apical and distal
inferior walls, and compensatory hyperkinesis of the basal anterior and
basal inferior walls. The systolic frames of the left ventriculogram
revealed a bottleneck appearance, which is characteristic of the apical
ballooning syndrome (Figure 1C and 1D). The left ventricular end-diastolic
pressure was 12 mm Hg. There was no systolic gradient measured across the
left ventricular outflow tract or the aortic valve. The left ventricular
ejection fraction (LVEF) was calculated to be 45%.
Echocardiography
Dr. Jonathan J. Passeri: A transthoracic echocardiogram was also obtained,
which showed severe segmental left ventricular dysfunction involving the
septum, anteroseptal territory, and apex (Figure 2Figure 2Transthoracic
Echocardiogram., and videos 1 and 2, available with the full text of this
article at NEJM.org). The overall left ventricular systolic function was
mildly impaired. The estimated LVEF was 48%. There was mild mitral
regurgitation.
Takotsubo Cardiomyopathy
Dr. Rosenfield: This elderly, hypertensive woman had the sudden onset of
chest pain and ECG findings that were compatible with a myocardial
infarction with ST-segment elevation. She did not have clinically
significant coronary atherosclerotic obstructions. The left ventriculogram
and echocardiogram showed anterior akinesis with apical and distal inferior
hypokinesis. Laboratory-test results from the emergency department showed a
troponin level of 0.4 ng per milliliter, indicating a minimal increase, and
a normal creatine kinase level. These are classic findings of Takotsubo
cardiomyopathy, also known as the apical ballooning syndrome, stress
cardiomyopathy, or the broken-heart syndrome.16 The name comes from the
Japanese words tako (octopus) and tsubo (pot), which refer to a pot with a
narrow neck that is used as an octopus trap.
The typical findings on angiography are left ventricular systolic
dysfunction with ballooning of the apex, in conjunction with normal or
increased contraction of the basilar area; this combination creates a
bottleneck appearance. As in this patient, coronary-artery obstructions
either are not present or do not correlate with the area of left ventricular
dysfunction. The hallmarks of the clinical presentation include sudden
onset of chest discomfort, dyspnea, shock, and, occasionally, syncope. As in
this patient, the initial ECG shows ST-segment elevation, which usually
yields to T-wave inversion within hours. New, pathologic Q waves can be
present but are frequently transient. There is generally mild elevation in
biomarkers for myocardial necrosis, much less than expected considering the
degree of left ventricular dysfunction.17
Takotsubo cardiomyopathy occurs predominantly in postmenopausal women, such
as this patient, and it is classically precipitated by a highly stressful
emotional or physiological event. It has also been described in patients who
have cumulative episodes of psychological stress, which could have been the
case in this patient, in view of her dementia and repeated episodes of
agitation. In approximately one third of cases, the trigger is not readily
identifiable.
This patient did not have a pressure gradient across the left ventricular
outflow tract; however, the distinct left ventricular wall-motion
abnormalities can occasionally lead to intracavitary obstruction,
hypotension, and refractory heart failure.18 Congestive heart failure is
seen in about 20 to 45% of patients with Takotsubo cardiomyopathy, but shock
and death from cardiovascular causes are rare (<1% of patients). Although
they are uncommon, malignant arrhythmias such as ventricular tachycardia and
ventricular fibrillation have been described in association with the
syndrome.17 This patient did not have any of these complications.
It has been estimated that from 1 to 2% of patients presenting with acute
coronary syndromes have Takotsubo cardiomyopathy19; however, it most likely
is underrecognized. The incidence has steadily increased, from 1 recognized
case at our hospital 12 years ago to more than 25 cases per year now. This
is most likely due to a combination of increased recognition and a possible
increase in the incidence of this disorder.
Management of Takotsubo Cardiomyopathy
The prognosis of Takotsubo cardiomyopathy is favorable, and more than 90% of
patients will recover fully; therefore, management of the syndrome is
conservative. For this patient, treatment entailed the discontinuation of
heparin and eptifibatide, as well as the administration of beta-blockers to
reduce any effect of catecholamines. She was transitioned from intravenous
nitroglycerin to an angiotensin-converting–enzyme (ACE) inhibitor. ACE
inhibitors are the preferred agents for management of systolic dysfunction
and hypertension. Because of persistent hypertension, we added the
administration of a dihydropyridine calcium-channel blocker. The patient had
some nocturnal delirium and required antianxiety therapy. Short-term
anticoagulation is occasionally used to prevent thrombus formation in the
left ventricle, but it was not administered in this patient. She was
discharged on day 6 to an acute care rehabilitation hospital, although she
protested this, wishing to return home.
Shortly after discharge, the patient became agitated and was transferred
back to this hospital. She reported recurrent chest pain and was found to be
hypertensive. The ECG revealed persistent ST-segment elevations. The
troponin level remained slightly elevated, but less so than on her previous
admission. Her symptoms resolved over a period of 2 days, with control of
her blood pressure and, most important, of her agitation. She was discharged
home with in-home services. This second episode might have represented a
recurrent Takotsubo cardiomyopathy. Upward of 10% of patients have a
recurrence, and there is no known strategy to prevent a recurrence.
Two years later, the patient is 95 years of age; unfortunately, her dementia
has worsened. She is still receiving beta-blockers and ACE inhibitors.
There has been no recurrence of chest pain or other cardiac symptoms. An
electrocardiogram obtained 21 months after presentation showed complete
resolution of the ST-segment changes and restoration of R waves in leads V1,
V2, and V3. We did not have a reassessment of her LVEF.
Dr. Nancy Lee Harris (Pathology): Are there any questions?
Dr. Alasdair K. Conn (Emergency Medicine): We are fortunate in this hospital
that we can call the team that is involved with myocardial infarction with
ST-segment elevation and send the patient directly to the catheterization
laboratory. An emergency physician in the community hospital has to make the
decision about whether to initiate thrombolysis or transfer the patient,
with a possible delay in definitive treatment.
Dr. Rosenfield: Most patients with Takotsubo cardiomyopathy meet the
criteria for myocardial infarction with ST-segment elevation and should be
treated for such, including balancing the risks and benefits of thrombolytic
therapy and transfer for primary percutaneous intervention (PCI). According
to published guidelines, if PCI will not be available within 90 to 120
minutes after the first medical contact, thrombolytic therapy should be
administered. Takotsubo cardiomyopathy is much less common than myocardial
infarction with ST-segment elevation.
Dr. Harris: In view of the absence of coronary artery disease on this
admission, I wonder whether the reported myocardial infarction 4 years
earlier could have been another episode of Takotsubo cardiomyopathy,
possibly triggered by the stress of the surgery for colon cancer.
Anatomical Diagnosis
Apical ballooning syndrome (Takotsubo cardiomyopathy).
1 (共1页)
进入Medicalpractice版参与讨论
相关主题
some board questions about cardiology求助:脑血栓!!! (转载)
CK question needs help.几篇期刊文章
金氏王朝在武汉大学的复辟Inquiry about the calcium supplement for kindney malfunction patients
Re: 金氏王朝在武汉大学的复制Heart Disease and Stroke Statistics—2013 Update
some board questions about cardiology (转载)请教,买神末样的听诊器
求教:妈妈冠心病的治疗选择(附CT图)CK form 1 block 2 Q18 help needed
冠心病的检查的方法及危险【intern 日记】终于熬过第一周了
心律不齐的问题南山,看看这个
相关话题的讨论汇总
话题: st话题: segment话题: patient话题: elevation话题: coronary