Right Ventricular Performance During Exercise In Patients With Heart Failure
HFSA ePoster Library. Yaseyyedi A. 09/10/21; 343455; 222
Armaan Yaseyyedi

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Abstract
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Background: Transthyretin Amyloid Cardiomyopathy (ATTR-CM) is classically described in older patients with heart failure with preserved ejection fraction (HFpEF). Using our institutional amyloid registry, we sought to understand the prevalence and survival of patients who, at the time of diagnosis, had heart failure with reduced left ventricular ejection fraction (LVEF ≤ 40%) and compare their clinical course with those presenting with HFpEF.
Methods: This is a single-center retrospective cohort study of 508 patients diagnosed with wild-type (WT) or V122I variant ATTR-CM. Cox proportional hazards models and Kaplan-Meier Survival analyses were used to assess probability of transplant-free survival.
Results: In our study cohort (median age 77 [71,83], 86% male, 27% black, median eGFR 58 [46,73]]), one third presented with HFrEF (n= 170). At the time of diagnosis, ATTR-CM patients with HFrEF had significantly higher median NT-proBNP (4257 [2424,7757] vs. 2363 [1067, 4125] pg/ml, p<0.001) and cardiac troponin T (0.05 [0.03, 0.13] vs 0.03 [0.01, 0.07], p<0.001) compared to that in non-HFrEF patients. Patients who were AA WT (n=44, 46%) and V122I (n=115, 47%) were significantly more likely to present with HFrEF than those were Caucasian WT (n=349, 28%), p < 0.001. Also, ATTR-CM patients with HFrEF had worse survival compared to those with non-HFrEF (HR, 1.63[95% CI, 1.23-2.16, p<0.001, Fig 1A]. However, after adjusting for NT-proBNP, there was no significant difference in survival between the two groups (HR, 1.33[95% CI, 0.95-1.86, p=0.093 Fig 1B].
Conclusions: In our single-center experience, one-third of patients newly diagnosed with ATTR-CM presented with LVEF ≤40% at the time of diagnosis, implying that clinical suspicion for diagnosis of ATTR-CM should extend beyond HFpEF presentation. AA WT and V122I patients had a higher proportion of HFrEF at initial diagnosis than Caucasian WT. Upon adjusting for NT-proBNP, ATTR-CM patients with HFrEF had similar survival compared to those presenting with HFpEF.
Methods: This is a single-center retrospective cohort study of 508 patients diagnosed with wild-type (WT) or V122I variant ATTR-CM. Cox proportional hazards models and Kaplan-Meier Survival analyses were used to assess probability of transplant-free survival.
Results: In our study cohort (median age 77 [71,83], 86% male, 27% black, median eGFR 58 [46,73]]), one third presented with HFrEF (n= 170). At the time of diagnosis, ATTR-CM patients with HFrEF had significantly higher median NT-proBNP (4257 [2424,7757] vs. 2363 [1067, 4125] pg/ml, p<0.001) and cardiac troponin T (0.05 [0.03, 0.13] vs 0.03 [0.01, 0.07], p<0.001) compared to that in non-HFrEF patients. Patients who were AA WT (n=44, 46%) and V122I (n=115, 47%) were significantly more likely to present with HFrEF than those were Caucasian WT (n=349, 28%), p < 0.001. Also, ATTR-CM patients with HFrEF had worse survival compared to those with non-HFrEF (HR, 1.63[95% CI, 1.23-2.16, p<0.001, Fig 1A]. However, after adjusting for NT-proBNP, there was no significant difference in survival between the two groups (HR, 1.33[95% CI, 0.95-1.86, p=0.093 Fig 1B].
Conclusions: In our single-center experience, one-third of patients newly diagnosed with ATTR-CM presented with LVEF ≤40% at the time of diagnosis, implying that clinical suspicion for diagnosis of ATTR-CM should extend beyond HFpEF presentation. AA WT and V122I patients had a higher proportion of HFrEF at initial diagnosis than Caucasian WT. Upon adjusting for NT-proBNP, ATTR-CM patients with HFrEF had similar survival compared to those presenting with HFpEF.
Background: Transthyretin Amyloid Cardiomyopathy (ATTR-CM) is classically described in older patients with heart failure with preserved ejection fraction (HFpEF). Using our institutional amyloid registry, we sought to understand the prevalence and survival of patients who, at the time of diagnosis, had heart failure with reduced left ventricular ejection fraction (LVEF ≤ 40%) and compare their clinical course with those presenting with HFpEF.
Methods: This is a single-center retrospective cohort study of 508 patients diagnosed with wild-type (WT) or V122I variant ATTR-CM. Cox proportional hazards models and Kaplan-Meier Survival analyses were used to assess probability of transplant-free survival.
Results: In our study cohort (median age 77 [71,83], 86% male, 27% black, median eGFR 58 [46,73]]), one third presented with HFrEF (n= 170). At the time of diagnosis, ATTR-CM patients with HFrEF had significantly higher median NT-proBNP (4257 [2424,7757] vs. 2363 [1067, 4125] pg/ml, p<0.001) and cardiac troponin T (0.05 [0.03, 0.13] vs 0.03 [0.01, 0.07], p<0.001) compared to that in non-HFrEF patients. Patients who were AA WT (n=44, 46%) and V122I (n=115, 47%) were significantly more likely to present with HFrEF than those were Caucasian WT (n=349, 28%), p < 0.001. Also, ATTR-CM patients with HFrEF had worse survival compared to those with non-HFrEF (HR, 1.63[95% CI, 1.23-2.16, p<0.001, Fig 1A]. However, after adjusting for NT-proBNP, there was no significant difference in survival between the two groups (HR, 1.33[95% CI, 0.95-1.86, p=0.093 Fig 1B].
Conclusions: In our single-center experience, one-third of patients newly diagnosed with ATTR-CM presented with LVEF ≤40% at the time of diagnosis, implying that clinical suspicion for diagnosis of ATTR-CM should extend beyond HFpEF presentation. AA WT and V122I patients had a higher proportion of HFrEF at initial diagnosis than Caucasian WT. Upon adjusting for NT-proBNP, ATTR-CM patients with HFrEF had similar survival compared to those presenting with HFpEF.
Methods: This is a single-center retrospective cohort study of 508 patients diagnosed with wild-type (WT) or V122I variant ATTR-CM. Cox proportional hazards models and Kaplan-Meier Survival analyses were used to assess probability of transplant-free survival.
Results: In our study cohort (median age 77 [71,83], 86% male, 27% black, median eGFR 58 [46,73]]), one third presented with HFrEF (n= 170). At the time of diagnosis, ATTR-CM patients with HFrEF had significantly higher median NT-proBNP (4257 [2424,7757] vs. 2363 [1067, 4125] pg/ml, p<0.001) and cardiac troponin T (0.05 [0.03, 0.13] vs 0.03 [0.01, 0.07], p<0.001) compared to that in non-HFrEF patients. Patients who were AA WT (n=44, 46%) and V122I (n=115, 47%) were significantly more likely to present with HFrEF than those were Caucasian WT (n=349, 28%), p < 0.001. Also, ATTR-CM patients with HFrEF had worse survival compared to those with non-HFrEF (HR, 1.63[95% CI, 1.23-2.16, p<0.001, Fig 1A]. However, after adjusting for NT-proBNP, there was no significant difference in survival between the two groups (HR, 1.33[95% CI, 0.95-1.86, p=0.093 Fig 1B].
Conclusions: In our single-center experience, one-third of patients newly diagnosed with ATTR-CM presented with LVEF ≤40% at the time of diagnosis, implying that clinical suspicion for diagnosis of ATTR-CM should extend beyond HFpEF presentation. AA WT and V122I patients had a higher proportion of HFrEF at initial diagnosis than Caucasian WT. Upon adjusting for NT-proBNP, ATTR-CM patients with HFrEF had similar survival compared to those presenting with HFpEF.
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