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acute coronary syndrom
about 75 y old patient with typical chest-pain with irradiation of left shoulder, dyspnoea; high-risk-patient (diabetes mellitus type 2, arterial hypertension, hyperlipoproteinaemia). In ECG I found no specific signs for myocardial ischaemia; in TTE no myocardial movement disorder. Using strain-rate-analysis we found a posterior/inf. and small anteroseptal movement disorder. high-sensitive Troponin was positive. In cardiac catheter we found a two vessel-desease (RCA, LAD) with leading high-grade stenosis of RCA.
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about 75 y old patient with typical chest-pain with irradiation of left shoulder, dyspnoea; high-risk-patient (diabetes mellitus type 2, arterial hypertension, hyperlipoproteinaemia). In ECG I found no specific signs for myocardial ischaemia; in TTE no myocardial movement disorder. Using strain-rate-analysis we found a posterior/inf. and small anteroseptal movement disorder. high-sensitive Troponin was positive. In cardiac catheter we found a two vessel-desease (RCA, LAD) with leading high-grade stenosis of RCA.
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cardial decompensation
about 80 y old patient with dyspnoea. The patient was admitted to our internal ER from surgical ward. Condition after implantation of VVI-pacemaker in context of bradyarrhythmia absoluta (actually the patient is pacemaker-dependent). In TTE we found us-b-lines and distinct pleural effusion right. There was alos a distinct decrease of cardial function, a severe pulmonary hypertension (RVSP about 65 mmHg) and a disorder of LV-compliance (approach to LVEDP about 20 mmHg; DecT 180 msec, E7A 2,3, E-velocity about 1 m/s, E`-velocity 0,5 m/sec, E/E´about 20 mmHg, Velocity-prolongation about 0,36 m/sec). IVC 19-20 mm without undulation.
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about 80 y old patient with dyspnoea. The patient was admitted to our internal ER from surgical ward. Condition after implantation of VVI-pacemaker in context of bradyarrhythmia absoluta (actually the patient is pacemaker-dependent). In TTE we found us-b-lines and distinct pleural effusion right. There was alos a distinct decrease of cardial function, a severe pulmonary hypertension (RVSP about 65 mmHg) and a disorder of LV-compliance (approach to LVEDP about 20 mmHg; DecT 180 msec, E7A 2,3, E-velocity about 1 m/s, E`-velocity 0,5 m/sec, E/E´about 20 mmHg, Velocity-prolongation about 0,36 m/sec). IVC 19-20 mm without undulation.
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cardiogenic shock caused by posterolateral-infarction (p-IABP implantation)
about 85 y old patient with STEMI. cardiac catheter showed an occlusion of ramus circumflecus. In TTE and TEE we could see an akinesia of posterolateral wall. In PA-cath: SVR 1200 dyn*s*cm^-5, CO 2,8 l/min, cardiac power 0,51 W: this is compatible to the clinical and echocardiographic picture of cardiogenic shock! This clip shows cardiac wall movemnt disorder and restricted cardiac ejection fraction prae-implantation of IABP.
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about 85 y old patient with STEMI. cardiac catheter showed an occlusion of ramus circumflecus. In TTE and TEE we could see an akinesia of posterolateral wall. In PA-cath: SVR 1200 dyn*s*cm^-5, CO 2,8 l/min, cardiac power 0,51 W: this is compatible to the clinical and echocardiographic picture of cardiogenic shock! This clip shows cardiac wall movemnt disorder and restricted cardiac ejection fraction prae-implantation of IABP.
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cardiogenic shock caused by thrombembolic occlusion of left main stem
about 75 y old patient with STEMI and about 45 minutes cpr. the patient was admitted from our ER after cardiac catheter to our ICU. In cardiac catheter we found a thrombotic occlusion of left main stem, no plaques and no stenosis. in clinical history a permanent atrial fibrillation with condition after several thrombembolic strokes is known. in TEE we found a distinct cardiac wall movement disorder of left ventricle and a small parietal residual of thrombus in LAA. we think that a thrombembolic cardiac infarction caused by thrombus in LAA is the most plausible reason of this finding.
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about 75 y old patient with STEMI and about 45 minutes cpr. the patient was admitted from our ER after cardiac catheter to our ICU. In cardiac catheter we found a thrombotic occlusion of left main stem, no plaques and no stenosis. in clinical history a permanent atrial fibrillation with condition after several thrombembolic strokes is known. in TEE we found a distinct cardiac wall movement disorder of left ventricle and a small parietal residual of thrombus in LAA. we think that a thrombembolic cardiac infarction caused by thrombus in LAA is the most plausible reason of this finding.
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Decompensation of stenosis of aortic valve (Part 2 of 3; Post-Valvuloplasty)
in part 2 you can see TEE immediate after Valvuloplasty: we were under the impression that the cardiac movement disorder are better oneself in comparison with cardiac movement disorder before valvuloplasty. The middle pressure gradient after valvuloplasty was only the half as before (about 20-25 mmHg; EF < 20%)
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in part 2 you can see TEE immediate after Valvuloplasty: we were under the impression that the cardiac movement disorder are better oneself in comparison with cardiac movement disorder before valvuloplasty. The middle pressure gradient after valvuloplasty was only the half as before (about 20-25 mmHg; EF < 20%)
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Mild LV-wall disturbance detected by speckle-pattern
About 45 y old patient with the typical clinical afflictions of acute coronary syndrom. in TTE I couldn´t see a LV-wall-motion-disorder. In Speckle-tracking/-pattern study I found a mild LV-wall-motion-disturbance. Troponin was positive. In coronary study we found a high-grade stenosis of RIVA compatible with the results of speckle-pattern-study. What do you think? Does anybody have any experiences with that kind of stuff? Is it a suitable kind of study?
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About 45 y old patient with the typical clinical afflictions of acute coronary syndrom. in TTE I couldn´t see a LV-wall-motion-disorder. In Speckle-tracking/-pattern study I found a mild LV-wall-motion-disturbance. Troponin was positive. In coronary study we found a high-grade stenosis of RIVA compatible with the results of speckle-pattern-study. What do you think? Does anybody have any experiences with that kind of stuff? Is it a suitable kind of study?
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Post-CPR
about 85 y old patient with severe acute RV-failure in context of chronic ischemic RV-failure. No sign of pulmonary embolism in initial TEE and ct-scan. First TTE we found a distinct RV-wall movement disorder. haemodynamic deteriorated rapidly, so we had to start cardiac resusciation for 3 minutes. in TTE we could see a distinct rv-pressure-overload with systolic d-sign. Actually vasopressor and inotropics save the situation. Any other hints in treatment of acute RV-Failure except inotropics and/ or vasopressor?
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about 85 y old patient with severe acute RV-failure in context of chronic ischemic RV-failure. No sign of pulmonary embolism in initial TEE and ct-scan. First TTE we found a distinct RV-wall movement disorder. haemodynamic deteriorated rapidly, so we had to start cardiac resusciation for 3 minutes. in TTE we could see a distinct rv-pressure-overload with systolic d-sign. Actually vasopressor and inotropics save the situation. Any other hints in treatment of acute RV-Failure except inotropics and/ or vasopressor?
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Tachy-Cardiomyopathy
About 50 y old patient with atrial fibrillation (HR about 150-170/min); the patient told clinical afflictions in the course of time of 3 weeks. In TTE we found a distinct LV-motion disorder and decrease of LV-EF. After exclusion of thrombus in LAA by TEE we did the elektrical cardioversion. After 1 week we saw a distinct improvement of LV-function.
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About 50 y old patient with atrial fibrillation (HR about 150-170/min); the patient told clinical afflictions in the course of time of 3 weeks. In TTE we found a distinct LV-motion disorder and decrease of LV-EF. After exclusion of thrombus in LAA by TEE we did the elektrical cardioversion. After 1 week we saw a distinct improvement of LV-function.
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Tako Tsubo cardiomyopathy
about 50 y old patient with severe posttraumatic stress disorder caused by death of near relative. The patient was admitted to out ER/ ICU with distinct and typical clinical affliction of acute coronary syndrome. Troponine I 0,8 (normal till 0,023), CK 210 U/l. In ECG we could see repolarisation disturbance without signs of ST-elevations. In TTE you can see myocardial movent disorder of apical LV-wall like an apical ballooning. No disturbance of RV. No US-B-lines, no pleural effusion, no sign of LVOTO despite the echocardiographic picture of hyperdynamic basal LV-wall-segments. In cardiac catheter no sign of coronary disease; we could see in cardiac catheter the typical movement disorder of Tako-Tsubo-CM as we could see in TTE before. One question to the community: Is there ALWAYS a need for cardiac catheter if we see the typical echocardiographic picture of apical ballooning/ Tako-Tsubo-CM?
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about 50 y old patient with severe posttraumatic stress disorder caused by death of near relative. The patient was admitted to out ER/ ICU with distinct and typical clinical affliction of acute coronary syndrome. Troponine I 0,8 (normal till 0,023), CK 210 U/l. In ECG we could see repolarisation disturbance without signs of ST-elevations. In TTE you can see myocardial movent disorder of apical LV-wall like an apical ballooning. No disturbance of RV. No US-B-lines, no pleural effusion, no sign of LVOTO despite the echocardiographic picture of hyperdynamic basal LV-wall-segments. In cardiac catheter no sign of coronary disease; we could see in cardiac catheter the typical movement disorder of Tako-Tsubo-CM as we could see in TTE before. One question to the community: Is there ALWAYS a need for cardiac catheter if we see the typical echocardiographic picture of apical ballooning/ Tako-Tsubo-CM?
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