scholarly journals Exertional dyspnea after myocardial infarction: thinking beyond the diagnosis of heart failure

2018 ◽  
Vol 46 (11) ◽  
pp. 4769-4774
Author(s):  
Konstantinos Koutsampasopoulos ◽  
Savvas Grigoriadis ◽  
Ioannis Vogiatzis
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Aneurysm ◽  
Left Ventricular Myocardium ◽  
Inferior Wall ◽  
Delayed Presentation ◽  
Exertional Dyspnea ◽  
St Elevation

Introduction We herein present an unusual case of a pseudoaneurysm of the left ventricular myocardium, which is a rare and fatal complication of myocardial infarction. Case report A 64-year-old man with a history of bipolar disorder and arterial hypertension was hospitalized for delayed presentation ST-elevation myocardial infarction. He was admitted to our hospital 24 hours after symptom onset. Diagnostic coronary angiography revealed 95% stenosis at the distal third of the right coronary artery, and he underwent a primary percutaneous coronary intervention to the culprit lesion. Despite administration of a diuretic and optimization of other pharmaceutical treatment, his heart failure deteriorated. Electrocardiography showed a sinus rhythm with Q-wave formation in the inferior wall leads (II, III, aVF), T-wave inversion in the same leads, and borderline QT prolongation (QTc of 490 ms). No ST elevation suggestive of left ventricular aneurysm formation was noticed. Forty days later, cardiac ultrasound revealed a dyskinetic cavity (pseudoaneurysm) in continuity with the posterior–inferior wall of the myocardium, resulting in severe mitral valve regurgitation. Unfortunately, the patient died while awaiting surgical treatment. Conclusion Although most patients with left ventricular pseudoaneurysm have a relatively benign outcome, those with symptoms of heart failure must be urgently diagnosed and treated.

scholarly journals Successful Surgical Treatment of Postinfarction Rupture of Left Ventricular Myocardium

2020 ◽  
Vol 9 (1) ◽  
pp. 140-147
Author(s):  
M. K. Mazanov ◽  
N. I. Kharitonova ◽  
A. A. Baranov ◽  
S. Yu. Kambarov ◽  
N. M. Bikbova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Surgical Intervention ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Free Wall ◽  
Fatal Complication ◽  
Widespread Availability ◽  
Complications Of Myocardial Infarction

ABSTRACT. The rupture of the left ventricle free wall is one of the most dangerous complications of myocardial infarction. Due to the widespread availability of echocardiography method, the detection of this fatal complication and the number of lives saved after surgery grew. The survival of patients depends on early diagnosis, stabilization of the patient’s condition, promptness and tactics of surgical intervention. We report a case of successful closure of a rupture of the left ventricle free wall on the 15th day after myocardial infarction.

scholarly journals Culprit vessel: impact on short-term and long-term prognosis in patients with ST-elevation myocardial infarction

Open Heart ◽  
2018 ◽  
Vol 5 (2) ◽  
pp. e000852 ◽  
Author(s):  
Artin Entezarjou ◽  
Moman Aladdin Mohammad ◽  
Pontus Andell ◽  
Sasha Koul
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
High Risk ◽  
Left Ventricular ◽  
St Elevation Myocardial Infarction ◽  
Clinical Event ◽  
Left Ventricular Ejection ◽  
Increased Risk ◽  
St Elevation ◽  
The Impact

BackgroundST-elevation myocardial infarction (STEMI) occurs as a result of rupture of an atherosclerotic plaque in the coronary arteries. Limited data exist regarding the impact of culprit coronary vessel on hard clinical event rates. This study investigated the impact of culprit vessel on outcomes after primary percutaneous coronary intervention (PCI) of STEMI.MethodsA total of 29 832 previously cardiac healthy patients who underwent primary PCI between 2003 and 2014 were prospectively included from the Swedish Coronary Angiography and Angioplasty Registry and the Registry of Information and Knowledge about Swedish Heart Intensive care Admissions. Patients were stratified into three groups based on culprit vessel (right coronary artery (RCA), left anterior descending artery (LAD) and left circumflex artery (LCx)). The primary outcome was 1-year mortality. The secondary outcomes included 30-day and 5-year mortality, as well as heart failure, stroke, bleeding and myocardial reinfarction at 30 days, 1 year and 5 years. Univariable and multivariable analyses were done using Cox regression models.ResultsOne-year analyses revealed that LAD infarctions had the highest increased risk of death, heart failure and stroke compared with RCA infarctions, which had the lowest risk. Sensitivity analyses revealed that reduced left ventricular ejection fraction on discharge partially explained this increased relative risk in mortality. Furthermore, landmark analyses revealed that culprit vessel had no significant influence on 1-year mortality if a patient survived 30 days after myocardial infarction. Subgroup analyses revealed female sex and multivessel disease (MVD) as significant high-risk groups with respect to 1-year mortality.ConclusionsLAD and LCx infarctions had a relatively higher adjusted mortality rate compared with RCA infarctions, with LAD infarctions in particular being associated with an increased risk of heart failure, stroke and death. Culprit vessel had limited influence on mortality after 1 month. High-risk patient groups include LAD infarctions in women or with concomitant MVD.

Deloading of the Left Ventricle by Ventricular Assist Device Normalizes Increased Expression of Endothelin ET A Receptors But Not Endothelin-Converting Enzyme-1 in Patients With End-Stage Heart Failure

Circulation ◽  
2000 ◽  
Vol 102 (suppl_3) ◽  
Author(s):  
Henning Morawietz ◽  
Marten Szibor ◽  
Winfried Goettsch ◽  
Babett Bartling ◽  
Matthias Barton ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Transplantation ◽  
Ace Inhibitor ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Converting Enzyme ◽  
Ventricular Assist ◽  
End Stage Heart Failure ◽  
End Stage

Background —Ventricular assist devices (VAD) are implanted in patients with end-stage heart failure for bridging the time until heart transplantation, resulting in hemodynamic unloading of the failing heart, improved cardiac contractile and mitochondrial function, and reversal of cardiac hypertrophy. It is unknown whether VAD unloading may affect the cardiac endothelin (ET) system, which has been proposed as one of the putative pathomechanisms of heart failure. Methods and Results —With the use of standard-calibrated, competitive reverse-transcription–polymerase chain reaction mRNA expression of components of the ET system was analyzed in left ventricular myocardium from nonfailing donor hearts, from failing hearts without and with ACE inhibitor therapy, and from patients with end-stage heart failure at the time of VAD implantation and 103±15 days after VAD implantation during removal with subsequent heart transplantation. ET receptor A (ET A ) was markedly upregulated in failing human myocardium. This increased ET A expression was not affected by ACE inhibitor treatment but was normalized by VAD unloading. ET A expression before or after VAD implantation did not correlate with duration of VAD implantation or suppression of Pro-ANP mRNA. ET B mRNA expression was unaffected by heart failure or VAD. In contrast, increased ET-converting enzyme-1 mRNA and ET-1 peptide levels in failing myocardium were partially normalized by ACE inhibition but not by VAD unloading. Conclusions —We conclude that VAD implantation normalizes ET A expression in failing human left ventricular myocardium, probably as the result of the beneficial effects of VAD unloading.

Reductions of myocardial Na-K-ATPase activity and ouabain binding sites in heart failure: prevention by nadolol

1993 ◽  
Vol 265 (6) ◽  
pp. H2086-H2093 ◽  
Author(s):  
T. H. Fan ◽  
R. P. Frantz ◽  
H. Elam ◽  
S. Sakamoto ◽  
N. Imai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atpase Activity ◽  
Binding Sites ◽  
Early Stage ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Adrenergic Stimulation ◽  
Ouabain Binding ◽  
Systemic Hemodynamic

To study the changes in myocardial digitalis binding sites in heart failure, we measured myocardial ouabain binding sites, Na-K-adenosinetriphosphatase (ATPase) activity, and ventricular muscle mechanical responses to acetylstrophanthidin in dogs with right-heart failure (RHF) produced by tricuspid avulsion and pulmonary artery constriction. Sham-operated dogs were studied as the control. RHF produced a significant decrease in ouabain binding sites in the right and left ventricular myocardium, which was accompanied by a proportional decrease in Na-K-ATPase activity. However, RHF and sham-operated dogs did not differ in systemic hemodynamic or right ventricular trabeculate muscle isometric contractile responses to acetylstrophanthidin. To determine whether chronic beta-adrenergic stimulation contributed to the development of Na-K-ATPase downregulation, we administered nadolol (40 mg/day) to a separate group of dogs during an early stage of RHF development. Nadolol effectively prevented the reduction of myocardial ouabain binding sites that occurred in RHF. Thus we conclude that myocardial ouabain binding sites and Na-K-ATPase activity are reduced in dogs with experimental heart failure and that these changes probably occur as a result of the attendant heightened sympathetic activity.

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