Blanka Fischerová

Sleep Apnea Prevalence in Acute Myocardial Infarction - the Sleep Apnea in Post Acute Myocardial Infarction Patients (SAPAMI) Study

BACKGROUND While sleep apnea (SA) might be a modifiable cardiovascular risk factor, recent data suggest that SA is severely underdiagnosed in patients after acute myocardial infarction (MI). There is limited evidence about day-night variation of onset of MI on dependence of having SA. We therefore investigated the prevalence of SA and examined the day-night variation of onset of MI in acute MI patients. METHODS We prospectively studied 782 consecutive patients admitted to the hospital with the diagnosis of acute MI. All subjects underwent sleep evaluations using a portable device after at least 48 h post-admission. Using the apnea-hypopnea index (AHI), groups were defined as patients without SA (<5 events/h), mild SA (5-15 events/h), moderate SA (15-30 events/h), and severe SA (≥ 30 events/h). RESULTS Almost all patients (98%) underwent urgent coronary angiography and 91% of patients underwent primary PCI. Using a threshold of AHI ≥ 5 events/h, SA was present in 65.7% of patients after acute MI. Mild SA was present in 32.6%, moderate in 20.4% and severe in 12.7%. The day-night variation in the onset of MI in all groups of SA patients was similar to that observed in non-SA patients. From 6 AM to 12 PM, the frequency of MI was higher in both SA and non-SA patients, as compared to the interval from 12 AM to 6 AM (all p<0.05). CONCLUSION There is a high prevalence of SA in patients presenting with acute MI. Peak time of MI onset in SA patients was between 6 AM and noon, similar to that in the general population. Whether diagnosis and treatment of SA after MI will significantly improve outcomes in these patients remains to be determined.

A comparison of intervention with losartan or captopril in acute myocardial infarction

Angiotensin‐converting enzyme (ACE) inhibitors prolong life, lower the progression of heart failure, and decrease the need for hospitalizations in patients after myocardial infarctions. It is still unclear whether these effects could also be achieved by blocking the angiotensin II (ATII) type 1 receptor.

First dose hypotension after angiotensin converting enzyme inhibitor captopril and angiotensin II blocker losartan in patients with acute myocardial infarction

BACKGROUND First dose hypotension after the administration of an angiotensin-converting enzyme inhibitor in patients with acute myocardial infarction is one of the most important adverse events of this type of treatment. There is no information about first dose hypotension after angiotensin type 1-receptor blocker in this type of patient. AIM To compare the first dose responses to low dose captopril and losartan in patients with acute myocardial infarction. METHODS Single blind, randomised, multicentric, prospective study. Patients (n=320) with confirmed acute myocardial infarction, age >18 years, treated by direct percutaneous transluminal coronary angioplasty, thrombolysis and/or heparin, were randomised to receive a single dose of 6.25-12.5 mg captopril or 12.5-25 mg losartan within 24 h of hospital admission. Baseline laboratory and clinical examinations were performed before entering the study. Blood pressure monitoring started at hospital admission and continued for at least 8 h after the medication (second dose of captopril was given after 8 h). RESULTS The maximal blood pressure fall appeared about 1 h after the first dose of captopril and 3.5 h after the first dose of losartan. Patients in the captopril group had significantly higher incidence of asymptomatic hypotension (38%) than patients treated with losartan (24%) (P<0.001). No difference in hypotension requiring a change in medication was observed. CONCLUSION Low dose of losartan is safe for initiating therapy in patients with acute myocardial infarction within 24 h of hospital admission.

Comparison of Acoustic Densitometry and Dobutamine Echocardiography for an Assessment of Myocardial Viability

Aim: The aim of this study has been to compare acoustic densitometry and dobutamine echocardiography for an assessment of myocardial viability. Methods and results: Thirty‐four patients with coronary artery disease and dysfunctional myocardial segments, who were referred for myocardial revascularization, underwent a viability assessment using low‐dose dobutamine echocardiography and acoustic densitometry. Results of the two techniques were compared to follow‐up resting echocardiography. This follow‐up examination was performed at a mean of 3 months after successful revascularization in order to assess the recovery of function in revascularized, initially dysfunctional segments. Echocardiography was performed in standard views using 16‐segment model of the left ventricle. Viable myocardium was identified by the augmentation of systolic thickening of an abnormal segment by at least one grade during dobutamine infusion and by the value of the maximal amplitude of cyclic variation of integrated backscatter. Acoustic densitometry had the sensitivity and specificity to predict functional recovery 90% and 77%, respectively. Dobutamine echocardiography had the sensitivity and specificity to predict contractile reserve 83% and 81%, respectively. The results were statistically comparable. Concordance between these methods was 80%. Conclusion: Acoustic densitometry and dobutamine echocardiography did not statistically differ in the prediction of functional recovery dysfunctional myocardial segments after revascularization.

674 Assessment of myocardial viability by acoustic densitometry in patients with left ventricle dysfunction due to coronary artery disease

Aim: The purpose of our study was to assess whether acoustic densitometry could distinguish between viable and irreversible dysfunctional myocardium in patients with coronary artery disease before myocardial revascularization. Methods: Seventy patients with chronic coronary artery disease and dysfunctional myocardial segments before planned myocardial revascularization were examined by acoustic densitometry. Fifty four patients had revascularization of at least one coronary artery supplying dysfunctional segments. Control echocardiography of these patients was performed after 3 months after bypass surgery or percutaneous coronary intervention for assessing contractility of revascularized, initially dysfunctional myocardial segments. The dysfunctional segments were defined as viable if they exhibited improvement in their thickening after revascularization. Wall motion was scored using 16-segment model of left ventricle, acoustic densitometry was evaluated from parasternal long axis view, parasternal short axis view at the level of papilary muscles and apical four-chamber and two-chamber views. Amplitude of cyclic variation of integrated backscatter (CVIB) was evaluated from each dysfunctional segment. Optimal cut off value of CVIB for distinction between viable and irreversible dysfunctional myocardium was found using receiver operating characteristic curves. Results: Cut off values for anteroseptal, posterior, interventricular septal, lateral, inferior and anterior segments were 4,1; 4,3; 4,4; 4,2; 4,5; 4,0 and 4,2 decibels, respectively. Sensitivity, specificity, positive and negative predictive values for identification of myocardial viability by acoustic densitometry using this cut off values were 918%, 81%, 87%, and 86%, respectively. Conclusion: Acoustic densitometry can differentiate viable and irreversible dysfunctional myocardium in patients with coronary artery disease before myocardial revascularization.