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Παρασκευή 17 Οκτωβρίου 2008
Δευτέρα 13 Οκτωβρίου 2008
Journal Club 2/10/2008
Episodic syncope in hypertrophic cardiomyopathy: evidence for inappropriate vasodilation
K Prasad, L Williams, R Campbell, P M Elliott, W J McKenna and M Frenneaux
Heart 2008;94;1312-1317; Originally published online 24 Jul 2008; doi:10.1136/hrt.2008.141507
Symptoms of impaired consciousness (syncope and presyncope)
occur in 15–25% of patients with hypertrophic cardiomyopathy (HCM). In young patients a history of recurrent syncope is associated with an increased risk of sudden death.
Syncope usually occurs without warning or symptoms suggestive of the cause. Detailed investigations identify a probable mechanism in a minority, usually paroxysmal atrial fibrillation or ventricular tachycardia. In the majority however no likely mechanism is found despite repeated 24-hour ambulatory echocardiography (ECG) or patient-activated monitoring, exercise testing and invasive electrophysiological studies.
Empirical treatment with amiodarone, a pacemaker or an implantable cardioverter-defibrillator is commonly employed, but is often unsuccessful in relieving the symptoms.
We have previously observed that approximately 30% of patients with HCM have abnormal blood pressure response during maximal upright exercise.
This was due in the majority of patients to an exaggerated fall in systemic vascular resistance, possibly arising from abnormal activation of stretch-sensitive left ventricular mechanoreceptors, by a mechanism similar to that described in aortic stenosis.
However, in some patients an inadequate cardiac output response to exercise may be responsible. We hypothesised that abnormal vasodepressor-mediated hypotension may also occur during daily life in patients with HCM, and that this may
be an important mechanism of syncope when conventional
investigations fail to reveal a cause.
CONCLUSIONS
Episodic hypotension occurs during ordinary activity in HCM patients with symptoms of impaired consciousness and is associated with abnormal blood pressure responses during maximal exercise.
This hypotension was due to inappropriate vasodilation. Our data suggest that these episodes may be an important cause of syncope in HCM
++++++++++++++++++++++++++++++++++++++++++++++++++++++++
Abnormal papillary muscle morphology is
independently associated with increased left ventricular outflow tract obstruction in
hypertrophic cardiomyopathy
D H Kwon, R M Setser, M Thamilarasan, Z V Popovic, N G Smedira, P Schoenhagen, M J Garcia, H M Lever and M Y Desai
Heart 2008;94;1295-1301; originally published online 9 Aug 2007; doi:10.1136/hrt.2007.118018
Background: Abnormal papillary muscles (PM) are often found in hypertrophic cardiomyopathy (HCM).
Objective: To assess the relationship between morphological alterations of PM in patients with HCM and left ventricular outflow tract (LVOT) obstruction, using magnetic resonance imaging (MRI) and echocardiography.
Methods: Fifty-six patients with HCM (mean age 42 years (interquartile range 27, 51), 70% male) and 30 controls (mean age (42 (30, 53) years, 80% male) underwent MRI on a 1.5 T scanner (Siemens, Erlangen, Germany). Standard cine images were obtained in shortaxis (base to apex), along with two-, three- and fourchamber views. The presence of bifid PM (none, one or both) and anteroapical displacement of anterolateral PM was recorded by MRI and correlated with resting LVOT gradients obtained by echocardiography.
Results: Double bifid PM (70% vs 17%) and anteroapical displacement of anterolateral PM (77% vs 17%) were more prevalent in patients with HCM than in controls (p,0.001).
Subjects with anteroapically displaced PM and double bifid PM had higher resting LVOT gradients than controls (45 (6, 81) vs 12 (0, 12) mm Hg (p,0.01) and 42 (6, 64) vs 11 (0, 17) mm Hg (p=0.02), respectively. In patients with HCM, the odds ratio of having significant (>30 mm Hg) peak resting gradient was 7.1 (95% CI 1.4 to 36.7) for anteroapically displaced anterolateral PM and 10.4 (95% CI 1.2 to 91.2) for double bifid PM (both p=0.005), independent of septal thickness, use of b-blockers and/or calcium blockers and
resting heart rate.
Conclusions: Patients with HCM with abnormal PM have a higher degree of resting LVOT gradient, which is independent of septal thickness.
Patients with HCM with altered PM morphology—that is, anteroapical displacement of anterolateral PM or double bifid PMs, have a significantly higher prevalence of SAM or an elevated resting LVOT gradient, compared with those without.
The association between altered PMs and resting LVOT gradient appears to be independent of septal thickness, resting heart rate or use of drugs (b-blockers or calcium blockers, or both). A significant proportion of patients with HCM with abnormal PM morphology continued to have provocable LVOT gradient despite septal myectomy. Further prospective long-itudinal studies are required to determine if abnormal PM morphology is progressive and associated with adverse outcomes.
Also, it needs to be determined if surgical correction of abnormal PM morphology provides incremental value to septal myectomy/mitral valve repair alone.
+++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
Prevalence of exercise-induced left ventricular outflow tract obstruction in symptomatic patients with non-obstructive hypertrophic cardiomyopathy
J S Shah, M T T Esteban, R Thaman, R Sharma, B Mist, A Pantazis, D Ward, S K Kohli, S P Page, C Demetrescu, E Sevdalis, A Keren, D Pellerin, W J McKenna and P M Elliott
Heart 2008;94;1288-1294; originally published online 21 Nov 2007;
doi:10.1136/hrt.2007.126003
ABSTRACT
Background: Resting left ventricular outflow tract obstruction (LVOTO) occurs in 25% of patients with hypertrophic cardiomyopathy (HCM) and is an important cause of symptoms and disease progression. The prevalence and clinical significance of exercise induced LVOTO in patients with symptomatic non-obstructive HCM is uncertain.
Methods and results: 87 symptomatic patients (43.3 (13.7) years, 67.8% males) with HCM and no previously documented LVOTO (defined as a gradient >30 mm Hg) underwent echocardiography during upright cardiopulmonary exercise testing: 54 patients (62.1%; 95% CI 51.5
to 71.6) developed LVOTO during exercise (latent LVOTO); 33 (37.9%; 95% CI 28.4 to 48.5) had neither resting nor exercise LVOTO (non-obstructive).
Patients with latent LVOTO were more likely to have systolic anterior motion of the mitral valve (SAM) at rest (relative risk 2.1, 95% CI
1.2 to 3.8; p=0.01), and higher peak oxygen consumption (mean difference: 10.3%, 95% CI 2.1 to 18.5; p=0.02) than patients with non-obstructive HCM.
The only independent predictors of D gradient during exercise were a history of presyncope/syncope, incomplete/complete SAM at rest and Wigle score (all p,0.05). Subsequent invasive reduction of LVOTO in 10
patients with latent obstruction and drug refractory symptoms resulted in improved functional class and less syncope/presyncope (all p,0.05).
Conclusions: Approximately two-thirds of patients with symptomatic non-obstructive HCM have latent LVOTO.
This study suggests that all patients with symptomatic non-obstructive HCM should have exercise stress echocardiography.
Over 60% of symptomatic patients with apparently nonobstructive hypertrophic cardiomyopathy have obstruction during exercise.
A history of presyncope/syncope and the presence of SAM are associated with the greatest changes in exercise-induced gradients.
The identification of latent obstruction as a cause of exertional symptoms should prompt more
vigorous pharmacological therapy, using combinations of drugs (including disopyramide) that would not be routinely employed in patients with non-obstructive HCM.
The use of invasive gradient reduction strategies (alcohol septal ablation and surgical myectomy) in patients with large exercise-induced gradients refractory to medical therapy can substantially
improve symptom status, but require further study in prospectively evaluated cohorts. The paradoxical relation between peak oxygen consumption and exercise-induced obstruction is intriguing and warrants further investigation.
K Prasad, L Williams, R Campbell, P M Elliott, W J McKenna and M Frenneaux
Heart 2008;94;1312-1317; Originally published online 24 Jul 2008; doi:10.1136/hrt.2008.141507
Symptoms of impaired consciousness (syncope and presyncope)
occur in 15–25% of patients with hypertrophic cardiomyopathy (HCM). In young patients a history of recurrent syncope is associated with an increased risk of sudden death.
Syncope usually occurs without warning or symptoms suggestive of the cause. Detailed investigations identify a probable mechanism in a minority, usually paroxysmal atrial fibrillation or ventricular tachycardia. In the majority however no likely mechanism is found despite repeated 24-hour ambulatory echocardiography (ECG) or patient-activated monitoring, exercise testing and invasive electrophysiological studies.
Empirical treatment with amiodarone, a pacemaker or an implantable cardioverter-defibrillator is commonly employed, but is often unsuccessful in relieving the symptoms.
We have previously observed that approximately 30% of patients with HCM have abnormal blood pressure response during maximal upright exercise.
This was due in the majority of patients to an exaggerated fall in systemic vascular resistance, possibly arising from abnormal activation of stretch-sensitive left ventricular mechanoreceptors, by a mechanism similar to that described in aortic stenosis.
However, in some patients an inadequate cardiac output response to exercise may be responsible. We hypothesised that abnormal vasodepressor-mediated hypotension may also occur during daily life in patients with HCM, and that this may
be an important mechanism of syncope when conventional
investigations fail to reveal a cause.
CONCLUSIONS
Episodic hypotension occurs during ordinary activity in HCM patients with symptoms of impaired consciousness and is associated with abnormal blood pressure responses during maximal exercise.
This hypotension was due to inappropriate vasodilation. Our data suggest that these episodes may be an important cause of syncope in HCM
++++++++++++++++++++++++++++++++++++++++++++++++++++++++
Abnormal papillary muscle morphology is
independently associated with increased left ventricular outflow tract obstruction in
hypertrophic cardiomyopathy
D H Kwon, R M Setser, M Thamilarasan, Z V Popovic, N G Smedira, P Schoenhagen, M J Garcia, H M Lever and M Y Desai
Heart 2008;94;1295-1301; originally published online 9 Aug 2007; doi:10.1136/hrt.2007.118018
Background: Abnormal papillary muscles (PM) are often found in hypertrophic cardiomyopathy (HCM).
Objective: To assess the relationship between morphological alterations of PM in patients with HCM and left ventricular outflow tract (LVOT) obstruction, using magnetic resonance imaging (MRI) and echocardiography.
Methods: Fifty-six patients with HCM (mean age 42 years (interquartile range 27, 51), 70% male) and 30 controls (mean age (42 (30, 53) years, 80% male) underwent MRI on a 1.5 T scanner (Siemens, Erlangen, Germany). Standard cine images were obtained in shortaxis (base to apex), along with two-, three- and fourchamber views. The presence of bifid PM (none, one or both) and anteroapical displacement of anterolateral PM was recorded by MRI and correlated with resting LVOT gradients obtained by echocardiography.
Results: Double bifid PM (70% vs 17%) and anteroapical displacement of anterolateral PM (77% vs 17%) were more prevalent in patients with HCM than in controls (p,0.001).
Subjects with anteroapically displaced PM and double bifid PM had higher resting LVOT gradients than controls (45 (6, 81) vs 12 (0, 12) mm Hg (p,0.01) and 42 (6, 64) vs 11 (0, 17) mm Hg (p=0.02), respectively. In patients with HCM, the odds ratio of having significant (>30 mm Hg) peak resting gradient was 7.1 (95% CI 1.4 to 36.7) for anteroapically displaced anterolateral PM and 10.4 (95% CI 1.2 to 91.2) for double bifid PM (both p=0.005), independent of septal thickness, use of b-blockers and/or calcium blockers and
resting heart rate.
Conclusions: Patients with HCM with abnormal PM have a higher degree of resting LVOT gradient, which is independent of septal thickness.
Patients with HCM with altered PM morphology—that is, anteroapical displacement of anterolateral PM or double bifid PMs, have a significantly higher prevalence of SAM or an elevated resting LVOT gradient, compared with those without.
The association between altered PMs and resting LVOT gradient appears to be independent of septal thickness, resting heart rate or use of drugs (b-blockers or calcium blockers, or both). A significant proportion of patients with HCM with abnormal PM morphology continued to have provocable LVOT gradient despite septal myectomy. Further prospective long-itudinal studies are required to determine if abnormal PM morphology is progressive and associated with adverse outcomes.
Also, it needs to be determined if surgical correction of abnormal PM morphology provides incremental value to septal myectomy/mitral valve repair alone.
+++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
Prevalence of exercise-induced left ventricular outflow tract obstruction in symptomatic patients with non-obstructive hypertrophic cardiomyopathy
J S Shah, M T T Esteban, R Thaman, R Sharma, B Mist, A Pantazis, D Ward, S K Kohli, S P Page, C Demetrescu, E Sevdalis, A Keren, D Pellerin, W J McKenna and P M Elliott
Heart 2008;94;1288-1294; originally published online 21 Nov 2007;
doi:10.1136/hrt.2007.126003
ABSTRACT
Background: Resting left ventricular outflow tract obstruction (LVOTO) occurs in 25% of patients with hypertrophic cardiomyopathy (HCM) and is an important cause of symptoms and disease progression. The prevalence and clinical significance of exercise induced LVOTO in patients with symptomatic non-obstructive HCM is uncertain.
Methods and results: 87 symptomatic patients (43.3 (13.7) years, 67.8% males) with HCM and no previously documented LVOTO (defined as a gradient >30 mm Hg) underwent echocardiography during upright cardiopulmonary exercise testing: 54 patients (62.1%; 95% CI 51.5
to 71.6) developed LVOTO during exercise (latent LVOTO); 33 (37.9%; 95% CI 28.4 to 48.5) had neither resting nor exercise LVOTO (non-obstructive).
Patients with latent LVOTO were more likely to have systolic anterior motion of the mitral valve (SAM) at rest (relative risk 2.1, 95% CI
1.2 to 3.8; p=0.01), and higher peak oxygen consumption (mean difference: 10.3%, 95% CI 2.1 to 18.5; p=0.02) than patients with non-obstructive HCM.
The only independent predictors of D gradient during exercise were a history of presyncope/syncope, incomplete/complete SAM at rest and Wigle score (all p,0.05). Subsequent invasive reduction of LVOTO in 10
patients with latent obstruction and drug refractory symptoms resulted in improved functional class and less syncope/presyncope (all p,0.05).
Conclusions: Approximately two-thirds of patients with symptomatic non-obstructive HCM have latent LVOTO.
This study suggests that all patients with symptomatic non-obstructive HCM should have exercise stress echocardiography.
Over 60% of symptomatic patients with apparently nonobstructive hypertrophic cardiomyopathy have obstruction during exercise.
A history of presyncope/syncope and the presence of SAM are associated with the greatest changes in exercise-induced gradients.
The identification of latent obstruction as a cause of exertional symptoms should prompt more
vigorous pharmacological therapy, using combinations of drugs (including disopyramide) that would not be routinely employed in patients with non-obstructive HCM.
The use of invasive gradient reduction strategies (alcohol septal ablation and surgical myectomy) in patients with large exercise-induced gradients refractory to medical therapy can substantially
improve symptom status, but require further study in prospectively evaluated cohorts. The paradoxical relation between peak oxygen consumption and exercise-induced obstruction is intriguing and warrants further investigation.
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