OBJECTIVES: We analyzed the possible relation between the presence of a hospital admission delay (> or =24 h), undue physical effort or recurrence of anginal pain, alone or in combination, with the development of free wall rupture (FWR), septal rupture (SR) or papillary muscle rupture (PMR) in patients with an acute myocardial infarction (AMI). BACKGROUND: Physical activity as a trigger of FWR in AMI remains controversial, and its contribution to SR or PMR remains unknown. Moreover, the role of ischemia or reinfarction as an additional cause of rupture has not been explored. METHODS: The incidence of hospital admission delay > or =24 h with maintenance of some ambulatory activity and the incidence of postinfarction angina were analyzed in consecutive patients with a first AMI with (n = 225) or without rupture (n = 1,012 [control group]) over different time periods. RESULTS: An admission delay > or =24 h occurred in 27 (27.6%) of 98 patients with FWR, 47 (47.0%) of 100 with SR and 14 (51.9%) of 27 with PMR but in only 81 (8%) of 1,012 control patients (p < 0.0001). Information on undue in-hospital effort preceding rupture was available for 111 patients and was present in 17 (32.7%) of 52 with FWR, 9 (18.4%) of 49 with SR and 3 (30%) of 10 with PMR versus only 76 (7.5%) of 1,012 control patients (p < 0.001). Information on postinfarction anginal pain was available for 114 patients with rupture and occurred in 30 (56.6%) of 53 with FWR, 30 (60%) of 50 with SR and 4 (36.4%) of 11 with PMR versus 120 (11.9%) of 1,012 control patients (p < 0.0001). Mean age and incidence of male gender, hypertension, absence of heart failure, single-vessel disease or occlusion of the infarct-related artery were comparable among the groups with FWR, SR or PMR. CONCLUSIONS: Delayed hospital admission or undue in-hospital physical activity appears to increase the risk of rupture in patients prone to this complication (i.e., a first transmural AMI, absence of overt heart failure and advanced age); recurrence of ischemia/infarction emerges as a potential additional trigger in a proportion of these patients.
OBJECTIVES: We analyzed the possible relation between the presence of a hospital admission delay (> or =24 h), undue physical effort or recurrence of anginal pain, alone or in combination, with the development of free wall rupture (FWR), septal rupture (SR) or papillary muscle rupture (PMR) in patients with an acute myocardial infarction (AMI). BACKGROUND: Physical activity as a trigger of FWR in AMI remains controversial, and its contribution to SR or PMR remains unknown. Moreover, the role of ischemia or reinfarction as an additional cause of rupture has not been explored. METHODS: The incidence of hospital admission delay > or =24 h with maintenance of some ambulatory activity and the incidence of postinfarction angina were analyzed in consecutive patients with a first AMI with (n = 225) or without rupture (n = 1,012 [control group]) over different time periods. RESULTS: An admission delay > or =24 h occurred in 27 (27.6%) of 98 patients with FWR, 47 (47.0%) of 100 with SR and 14 (51.9%) of 27 with PMR but in only 81 (8%) of 1,012 control patients (p < 0.0001). Information on undue in-hospital effort preceding rupture was available for 111 patients and was present in 17 (32.7%) of 52 with FWR, 9 (18.4%) of 49 with SR and 3 (30%) of 10 with PMR versus only 76 (7.5%) of 1,012 control patients (p < 0.001). Information on postinfarction anginal pain was available for 114 patients with rupture and occurred in 30 (56.6%) of 53 with FWR, 30 (60%) of 50 with SR and 4 (36.4%) of 11 with PMR versus 120 (11.9%) of 1,012 control patients (p < 0.0001). Mean age and incidence of male gender, hypertension, absence of heart failure, single-vessel disease or occlusion of the infarct-related artery were comparable among the groups with FWR, SR or PMR. CONCLUSIONS: Delayed hospital admission or undue in-hospital physical activity appears to increase the risk of rupture in patients prone to this complication (i.e., a first transmural AMI, absence of overt heart failure and advanced age); recurrence of ischemia/infarction emerges as a potential additional trigger in a proportion of these patients.