467
edits
Myocardial and Pericardial Disease: Difference between revisions
Myocardial and Pericardial Disease (view source)
Revision as of 20:24, 4 October 2012
, 4 October 2012no edit summary
No edit summary |
No edit summary |
||
| Line 753: | Line 753: | ||
In patients with medically refractory symptoms, whom are suboptimal candidates for invasive treatment, permanent dual chamber pacing may be considered. Pacing may alleviate symptoms by decreasing the outflow tract pressure gradient. However, maintaining a reduction in gradient requires pre-exitation of the right ventricular apex and distal septum, and complete ventricular caption. For optimal results, this should therefore be performed in highly experienced centers only. | In patients with medically refractory symptoms, whom are suboptimal candidates for invasive treatment, permanent dual chamber pacing may be considered. Pacing may alleviate symptoms by decreasing the outflow tract pressure gradient. However, maintaining a reduction in gradient requires pre-exitation of the right ventricular apex and distal septum, and complete ventricular caption. For optimal results, this should therefore be performed in highly experienced centers only. | ||
[[Image:Myocardi1.jpg| | [[Image:Myocardi1.jpg|400px|thumb|Figure 1. Treatment strategy in HCM]] | ||
=====Prognosis and outcome===== | =====Prognosis and outcome===== | ||
| Line 795: | Line 795: | ||
In general, a wide variety of factors can induce or contribute to the development of DCM including arterial hypertension, myocarditis, alcohol abuse or tachyarrhythmias. A subsequent increase in wall stress combined with activation of neurohumoral pathways induces complex cellular and molecular maladaptation, and programmed cell death finally leads to a decrease in the number of functioning cardiomyocytes. This process of cardiac remodelling itself results in systolic and/or diastolic dysfunction, leading to increased wall stress, and thereby creating a vicious circle of progressive systolic dysfunction (Figure 1). | In general, a wide variety of factors can induce or contribute to the development of DCM including arterial hypertension, myocarditis, alcohol abuse or tachyarrhythmias. A subsequent increase in wall stress combined with activation of neurohumoral pathways induces complex cellular and molecular maladaptation, and programmed cell death finally leads to a decrease in the number of functioning cardiomyocytes. This process of cardiac remodelling itself results in systolic and/or diastolic dysfunction, leading to increased wall stress, and thereby creating a vicious circle of progressive systolic dysfunction (Figure 1). | ||
[[Image:Process of cardiac remodelling.png|thumb|400px|Figure 1 | [[Image:Process of cardiac remodelling.png|thumb|400px|Figure 1]] | ||
The failing myocardium has several distinct factors promoting apoptosis of cardiomyocytes in vitro; cathecholamines, wall stress, angiotensin II, nitric oxide and inflammatory cytokines. Hence, medical management of DCM aims at antagonizing these pathways, reducing stress signalling in, and remodelling of the failing heart. | The failing myocardium has several distinct factors promoting apoptosis of cardiomyocytes in vitro; cathecholamines, wall stress, angiotensin II, nitric oxide and inflammatory cytokines. Hence, medical management of DCM aims at antagonizing these pathways, reducing stress signalling in, and remodelling of the failing heart. | ||
| Line 1,226: | Line 1,226: | ||
|Normal wall thickness | |Normal wall thickness | ||
|Pericardial thickening | |Pericardial thickening | ||
|- | |||
|- | |- | ||
|Diastolic notch of interventricular septum | |Diastolic notch of interventricular septum | ||
|- | |||
|Increased wall thickness (amyloidosis) | |Increased wall thickness (amyloidosis) | ||
|Enlarged left and right atria | |Enlarged left and right atria | ||
|- | |||
|Doppler studies e' septal =8 cm/sec and normal S' mitral annular velocity | |Doppler studies e' septal =8 cm/sec and normal S' mitral annular velocity | ||
|- | |||
|Mitral inflow increase during expiration | |Mitral inflow increase during expiration | ||
Mitral flow propagation velocity M-mode colour =45cm/s | |||
hepatic vein with expiration e' septal <8cm/s and decreased mitral annular velocity | |||
Increased diastolic flow reversal in the hepatic vein with expiration e' septal <8cm/s and decreased mitral annular velocity | |||
|Mitral inflow velocity without respiratory variation | |Mitral inflow velocity without respiratory variation | ||
Mitral flow propagation velocity M-mode colour <45cm/s | |||
Increased diastolic flow reversal in the hepatic vein with inspiration | |||
|- | |||
|Cardiac catheterization | |Cardiac catheterization | ||
|- | |||
|RVEDP and LVEDP usually equal | |RVEDP and LVEDP usually equal | ||
RV systolic pressure <50mmHg | |||
|RVEDP >one-third of RV systolic pressure | |RVEDP >one-third of RV systolic pressure | ||
LVEDP often >5mm greater than RVEDP | |||
|- | |||
|Endomyocardial biopsy | |Endomyocardial biopsy | ||
|- | |||
|Normal or non-specific changes | |Normal or non-specific changes | ||
|May reveal specific causes | |May reveal specific causes | ||
|- | |||
|CT/MR imaging | |CT/MR imaging | ||
|- | |||
|Pericardium thickened or calcified | |||
|Normal pericardium | |||
|- | |||
|CT, computer tomography; | |||
|- | |||
|e', e wave velocity by tissue velocity imaging; | |||
LVEDP, left ventricular end-diastolic pressure; | |||
MR, magnetic resonance; | |||
|RV, right ventricular; | |||
RVEDP, right ventricular end-diastolic pressure. | |||
|} | |} | ||