ß-blockers after myocardial infarction and 1-year clinical outcome - a retrospective study.

BACKGROUND: Long term ß-blocker therapy after myocardial infarction (MI) reduces mortality and recurrent MI but evidence for this treatment predates contemporary acute coronary care. ß-blocker treatment is a key quality of care indicator in the Swedish national quality register for acute coronary care, Riks-HIA. Between 2011 and 2015 a declining number of MI-patients discharged with a ß-blocker from the coronary care unit (CCU) at Helsingborg and other hospitals was reported. This retrospective observational study aimed to investigate the causes for discharge without a ß-blocker and relate it to outcome, compared to patients discharged with a ß-blocker. METHODS: MI-patients registered in Riks-HIA discharged without ß-blocker during 2011-2015 (no-ß-group) and a control group (ß-group) comprised of patients discharged with ß-blocker treatment between January 1 to December 31, 2013, were matched by RIKS-HIA criteria for ß-blocker use. Clinical characteristics, date of death, readmission for MI, other cardiovascular events were collected from Riks-HIA and medical records. RESULTS: The no-ß-group included 141 patients, where 65.2% had a justified reason for non-ß-blocker use. The ß-group included 206 patients. There was no difference in cardiovascular risk factor profile. There were a trend towards a higher number of readmissions for MI in the no-ß-group was (n = 8 (5.7%) vs n = 2 (1.0%), p = 0.02), but not mortality (6 (4.3%) vs 2 (1.0%), p = 0.07) and combined readmission for angina pectoris, heart failure, arrhythmias or stroke/TIA (n = 23 (16.3%) vs n = 25 (12.1%), p = 0.27). CONCLUSION: A majority of the patients in the no-ß-group had a justified absence of a ß-blocker. ß-blocker treatment post-MI showed a trend towards fewer readmissions for MI. But important quality information is lacking to make a firm conclusion of the effect on outcome.

Mechanical chest compressions for cardiac arrest in the cath-lab: when is it enough and who should go to extracorporeal cardio pulmonary resuscitation?

BACKGROUND: Treating patients in cardiac arrest (CA) with mechanical chest compressions (MCC) during percutaneous coronary intervention (PCI) is now routine in many coronary catheterization laboratories (cath-lab) and more aggressive treatment modalities, including extracorporeal CPR are becoming more common. The cath-lab setting enables monitoring of vital physiological parameters and other clinical factors that can potentially guide the resuscitation effort. This retrospective analysis attempts to identify such factors associated with ROSC and survival. METHODS: In thirty-five patients of which background data, drugs used during the resuscitation and the intervention, PCI result, post ROSC-treatment and physiologic data collected during CPR were compared for prediction of ROSC and survival. RESULTS: Eighteen (51%) patients obtained ROSC and 9 (26%) patients survived with good neurological outcome. There was no difference between groups in regards of background data. Patients arriving in the cath-lab with ongoing resuscitation efforts had lower ROSC rate (22% vs 53%; p = 0.086) and no survivors (0% vs 50%, p = 0.001). CPR time also differentiated resuscitation outcomes (ROSC: 18 min vs No ROSC: 50 min; p = 0.007 and Survivors: 10 min vs No Survivors: 45 min; p = 0.001). Higher arterial diastolic blood pressure was associated with ROSC: 30 mmHg vs No ROSC: 19 mmHg; p = 0.012). CONCLUSION: Aortic diastolic pressure during CPR is the most predictive physiological parameter of resuscitation success. Ongoing CPR upon arrival at the cath-lab and continued MCC beyond 10-20 min in the cath-lab were both predictive of poor outcomes. These factors can potentially guide decisions regarding escalation and termination of resuscitation efforts.

Assessment of increasing intravenous adenosine dose in fractional flow reserve.

BACKGROUND: Effects of increased adenosine dose in the assessment of fractional flow reserve (FFR) were studied in relation to FFR results, hemodynamic effects and patient discomfort. FFR require maximal hyperemia mediated by adenosine. Standard dose is 140 µg/kg/min administrated intravenously. Higher doses are commonly used in clinical practice, but an extensive comparison between standard intravenous dose and a high dose (220 µg/kg/min) has previously not been performed. METHODS: Seventy-five patients undergoing FFR received standard dose adenosine, followed by high dose adenosine. FFR, mean arterial pressure (MAP) and heart rate (HR) were analyzed. Patient discomfort measured by Visual Analogue Scale (VAS) was assessed. RESULTS: No significant difference was found between the doses in FFR value (0.85 [0.79-0.90] vs 0.85 [0.79-0.89], p = 0.24). The two doses correlated well irrespective of lesion severity (r = 0.86, slope = 0.89, p = <0.001). There were no differences in MAP or HR. Patient discomfort was more pronounced using high dose adenosine (8.0 [5.0-9.0]) versus standard dose (5.0 [2.0-7.0]), p = <0.001. CONCLUSIONS: Increased dose adenosine does not improve hyperemia and is associated with increased patient discomfort. Our findings do not support the use of high dose adenosine. TRIAL REGISTRATION: Retrospective Trial registration: Current Controlled Trials ISRCTN14618196 . Registered 15 December 2016.

Repeated epinephrine doses during prolonged cardiopulmonary resuscitation have limited effects on myocardial blood flow: a randomized porcine study.

BACKGROUND: In current guidelines, prolonged cardiopulmonary resuscitation (CPR) mandates administration of repeated intravenous epinephrine (EPI) doses. This porcine study simulating a prolonged CPR-situation in the coronary catheterisation laboratory, explores the effect of EPI-administrations on coronary perfusion pressure (CPP), continuous coronary artery flow average peak velocity (APV) and amplitude spectrum area (AMSA). METHODS: Thirty-six pigs were randomized 1:1:1 to EPI 0.02 mg/kg/dose, EPI 0.03 mg/kg/dose or saline (control) in an experimental cardiac arrest (CA) model. During 15 minutes of mechanical chest compressions, four EPI/saline-injections were administered, and the effect on CPP, APV and AMSA were recorded. Comparisons were performed between the control and the two EPI-groups and a combination of the two EPI-groups, EPI-all. RESULT: Compared to the control group, maximum peak of CPP (Pmax) after injection 1 and 2 was significantly increased in the EPI-all group (p = 0.022, p = 0.016), in EPI 0.02-group after injection 2 and 3 (p = 0.023, p = 0.027) and in EPI 0.03-group after injection 1 (p = 0.013). At Pmax, APV increased only after first injection in both the EPI-all and the EPI 0.03-group compared with the control group (p = 0.011, p = 0.018). There was no statistical difference of AMSA at any Pmax. Seven out of 12 animals (58%) in each EPI-group versus 10 out of 12 (83%) achieved spontaneous circulation after CA. CONCLUSION: In an experimental CA-CPR pig model repeated doses of intravenous EPI results in a significant increase in APV only after the first injection despite increments in CPP also during the following 2 injections indicating inappropriate changes in coronary vascular resistance during subsequent EPI administration.

Evaluation of coronary blood flow velocity during cardiac arrest with circulation maintained through mechanical chest compressions in a porcine model.

BACKGROUND: Mechanical chest compressions (CCs) have been shown capable of maintaining circulation in humans suffering cardiac arrest for extensive periods of time. Reports have documented a visually normalized coronary blood flow during angiography in such cases (TIMI III flow), but it has never been actually measured. Only indirect measurements of the coronary circulation during cardiac arrest with on-going mechanical CCs have been performed previously through measurement of the coronary perfusion pressure (CPP). In this study our aim was to correlate average peak coronary flow velocity (APV) to CPP during mechanical CCs. METHODS: In a closed chest porcine model, cardiac arrest was established through electrically induced ventricular fibrillation (VF) in eleven pigs. After one minute, mechanical chest compressions were initiated and then maintained for 10 minutes upon which the pigs were defibrillated. Measurements of coronary blood flow in the left anterior descending artery were made at baseline and during VF with a catheter based Doppler flow fire measuring APV. Furthermore measurements of central (thoracic) venous and arterial pressures were also made in order to calculate the theoretical CPP. RESULTS: Average peak coronary flow velocity was significantly higher compared to baseline during mechanical chests compressions and this was observed during the entire period of mechanical chest compressions (12 - 39% above baseline). The APV slowly declined during the 10 min period of mechanical chest compressions, but was still higher than baseline at the end of mechanical chest compressions. CPP was simultaneously maintained at > 20 mmHg during the 10 minute episode of cardiac arrest. CONCLUSION: Our study showed good correlation between CPP and APV which was highly significant, during cardiac arrest with on-going mechanical CCs in a closed chest porcine model. In addition APV was even higher during mechanical CCs compared to baseline. Mechanical CCs can, at minimum, re-establish coronary blood flow in non-diseased coronary arteries during cardiac arrest.

Arrhythmia-provoking factors and symptoms at the onset of paroxysmal atrial fibrillation: a study based on interviews with 100 patients seeking hospital assistance.

BACKGROUND: Surprisingly little information on symptoms of paroxysmal atrial fibrillation is available in scientific literature. Using questionnaires, we have analyzed the symptoms associated with arrhythmia attacks. METHODS: One hundred randomly-selected patients with idiopathic paroxysmal atrial fibrillation filled in a structured questionnaire. RESULTS: Psychic stress was the most common factor triggering arrhythmia (54%), followed by physical exertion (42%), tiredness (41%) coffee (25%) and infections (22%). Thirty-four patients cited alcohol, 26 in the form of red wine, 16 as white wine and 26 as spirits. Among these 34, red wine and spirits produced significantly more episodes of arrhythmia than white wine (p = 0.01 and 0.005 respectively). Symptoms during arrhythmia were palpitations while exerting (88%), reduced physical ability (87%), palpitations at rest (86%), shortage of breath during exertion (70%) and anxiety (59%). Significant differences between sexes were noted regarding swollen legs (women 21%, men 6%, p = 0.027), nausea (women 36%, men 13%, p = 0.012) and anxiety (females 79%, males 51%, p = 0.014). CONCLUSION: Psychic stress was the commonest triggering factor in hospitalized patients with paroxysmal atrial fibrillation. Red wine and spirits were more proarrhythmic than white wine. Symptoms in women in connection with attacks of arrhythmia vary somewhat from those in men.

The analgesic effect of oxygen during percutaneous coronary intervention (the OXYPAIN Trial).

INTRODUCTION: Oxygen is considered to have analgesic effects, but the evidence is weak. Oxygen may be harmful to the ischemic myocardium. The aim was to investigate the analgesic effect of oxygen during percutaneous coronary intervention (PCI) and to evaluate cardiac injury. MATERIAL AND METHODS: The OXYPAIN was a phase II randomized trial with a double blind design. 305 patients were randomized to receive oxygen or atmospheric air during PCI. The patients were asked to score chest pain by the Visual-Analog Scale (VAS). The use of analgesic agents and troponin-t was measured. RESULTS: There was no significant difference in pain between the groups: oxygen: 2.0, [2.0-4.0], air: 2.0, [2.0-5.0] (median, interquartile range: 25-75%, P = 0.12). The median difference in score of VAS was [95% CI]: 0, [0-1.0]. The oxygen group received 0.44 ± 0.11 mg of morphine versus 0.46 ± 0.13, P = n.s. The peak value of troponin-t post-PCI was 38, [11-352] nmol/ml in the oxygen group and 61, [16-241] for patients treated with air, P = 0.46. CONCLUSIONS: The use of oxygen during PCI did not demonstrate any analgesic effect. There was no difference in myocardial injury measured with troponin-t or in the morphine dose. Our results do not support routine use of oxygen. (NCT01413841.).