Randomized controlled trial of an intervention to change cardiac misconceptions in myocardial infarction patients

There is converging evidence that changing beliefs about an illness leads to positive recovery outcomes. However, cardiac misconceptions interventions have been investigated mainly in Angina or Coronary Heart Disease patients, and less in patients following Myocardial Infarction (MI). In these patients, cardiac misconceptions may play a role in the adjustment or lifestyle changes. This article reports a randomized controlled trial of an intervention designed to reduce the strength of misconceptions in patients after a first MI. The primary outcome was the degree of change in misconceptions and the secondary outcomes were: exercise, smoking status, return to work and mood (anxiety and depression). Patients in the intervention condition (n = 60) were compared with a control group (n = 67) receiving usual care. Both groups were evaluated at baseline and 4, 8 and 12 months after hospital discharge. There was a significant time-by-group interaction for the total score of cardiac misconceptions. Patients in the intervention group significantly decreased their total score of cardiac misconceptions at 4 months compared with the control group and this difference was sustained over time. Patients in the intervention group were also more likely to exercise at the follow-up period after MI than the control group. This intervention was effective in reducing the strength of cardiac misconceptions in MI patients and had a positive impact on health behaviour outcomes. These results support the importance of misconceptions in health behaviours and the utility of belief change interventions in promoting health in patients with Myocardial Infarction.

Women's experiences of how their recovery process is promoted after a first myocardial infarction : Implications for cardiac rehabilitation care

Background: After a myocardial infarction and discharge from the hospital a recovery process follows for the women. In order to facilitate their recovery, both a preventive and promotive perspective should be taken into consideration. Despite this, today´s healthcare focuses more on prevention and thus research into the promotion of women’s recovery process is needed. Aim: To explore how women’s recovery processes are promoted after a first myocardial infarction Methods: The study had an explorative and descriptive design based on qualitative content analysis. Findings: The women’s recovery process was promoted through using external and internal resources as well as embracing behaviour, social and psychological dimensions. The women embraced these dimensions to a varying extent and this process led to them being able to take in a new perspective on life. Conclusions: The women’s personal recovery is a multidirectional process with a desire to develop and approach a new perspective on life. It is important for cardiac rehabilitation nurses to not only focus on lifestyle changes and social support, but also on working actively with the women’s inner strength in order to promote the personal recovery of the women. Furthermore, it would be interesting to investigate men’s experiences of how their recovery process after a first Myocardial infarction is promoted.

Long-term benefit of early pre-reperfusion metoprolol administration in patients with acute myocardial infarction: Results from the Metocard-CNIC trial (Effect of Metoprolol in Cardioprotection during an Acute Myocardial Infarction)

The goal of this trial was to study the long-term effects of intravenous (IV) metoprolol administration before reperfusion on left ventricular (LV) function and clinical events. Early IV metoprolol during ST-segment elevation myocardial infarction (STEMI) has been shown to reduce infarct size when used in conjunction with primary percutaneous coronary intervention (pPCI). The METOCARD-CNIC (Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction) trial recruited 270 patients with Killip class ≤II anterior STEMI presenting early after symptom onset (<6 h) and randomized them to pre-reperfusion IV metoprolol or control group. Long-term magnetic resonance imaging (MRI) was performed on 202 patients (101 per group) 6 months after STEMI. Patients had a minimal 12-month clinical follow-up. Left ventricular ejection fraction (LVEF) at the 6 months MRI was higher after IV metoprolol (48.7 ± 9.9% vs. 45.0 ± 11.7% in control subjects; adjusted treatment effect 3.49%; 95% confidence interval [CI]: 0.44% to 6.55%; p = 0.025). The occurrence of severely depressed LVEF (≤35%) at 6 months was significantly lower in patients treated with IV metoprolol (11% vs. 27%, p = 0.006). The proportion of patients fulfilling Class I indications for an implantable cardioverter-defibrillator (ICD) was significantly lower in the IV metoprolol group (7% vs. 20%, p = 0.012). At a median follow-up of 2 years, occurrence of the pre-specified composite of death, heart failure admission, reinfarction, and malignant arrhythmias was 10.8% in the IV metoprolol group versus 18.3% in the control group, adjusted hazard ratio (HR): 0.55; 95% CI: 0.26 to 1.04; p = 0.065. Heart failure admission was significantly lower in the IV metoprolol group (HR: 0.32; 95% CI: 0.015 to 0.95; p = 0.046). In patients with anterior Killip class ≤II STEMI undergoing pPCI, early IV metoprolol before reperfusion resulted in higher long-term LVEF, reduced incidence of severe LV systolic dysfunction and ICD indications, and fewer heart failure admissions.

Myocardial edema after ischemia/reperfusion is not stable and follows a bimodal pattern: Imaging and histological tissue characterization

It is widely accepted that edema occurs early in the ischemic zone and persists in stable form for at least 1 week after myocardial ischemia/reperfusion. However, there are no longitudinal studies covering from very early (minutes) to late (1 week) reperfusion stages confirming this phenomenon. This study sought to perform a comprehensive longitudinal imaging and histological characterization of the edematous reaction after experimental myocardial ischemia/reperfusion. The study population consisted of 25 instrumented Large-White pigs (30 kg to 40 kg). Closed-chest 40-min ischemia/reperfusion was performed in 20 pigs, which were sacrificed at 120 min (n = 5), 24 h (n = 5), 4 days (n = 5), and 7 days (n = 5) after reperfusion and processed for histological quantification of myocardial water content. Cardiac magnetic resonance (CMR) scans with T2-weighted short-tau inversion recovery and T2-mapping sequences were performed at every follow-up stage until sacrifice. Five additional pigs sacrificed after baseline CMR served as controls. In all pigs, reperfusion was associated with a significant increase in T2 relaxation times in the ischemic region. On 24-h CMR, ischemic myocardium T2 times returned to normal values (similar to those seen pre-infarction). Thereafter, ischemic myocardium-T2 times in CMR performed on days 4 and 7 after reperfusion progressively and systematically increased. On day 7 CMR, T2 relaxation times were as high as those observed at reperfusion. Myocardial water content analysis in the ischemic region showed a parallel bimodal pattern: 2 high water content peaks at reperfusion and at day 7, and a significant decrease at 24 h. Contrary to the accepted view, myocardial edema during the first week after ischemia/reperfusion follows a bimodal pattern. The initial wave appears abruptly upon reperfusion and dissipates at 24 h. Conversely, the deferred wave of edema appears progressively days after ischemia/reperfusion and is maximal around day 7 after reperfusion.

Early intravenous beta-blockers in patients with ST-segment elevation myocardial infarction before primary percutaneous coronary intervention

The impact of intravenous (IV) beta-blockers before primary percutaneous coronary intervention (PPCI) on infarct size and clinical outcomes is not well established. This study sought to conduct the first double-blind, placebo-controlled international multicenter study testing the effect of early IV beta-blockers before PPCI in a general ST-segment elevation myocardial infarction (STEMI) population. STEMI patients presenting <12 h from symptom onset in Killip class I to II without atrioventricular block were randomized 1:1 to IV metoprolol (2 × 5-mg bolus) or matched placebo before PPCI. Primary endpoint was myocardial infarct size as assessed by cardiac magnetic resonance imaging (CMR) at 30 days. Secondary endpoints were enzymatic infarct size and incidence of ventricular arrhythmias. Safety endpoints included symptomatic bradycardia, symptomatic hypotension, and cardiogenic shock. A total of 683 patients (mean age 62 ± 12 years; 75% male) were randomized to metoprolol (n = 336) or placebo (n = 346). CMR was performed in 342 patients (54.8%). Infarct size (percent of left ventricle [LV]) by CMR did not differ between the metoprolol (15.3 ± 11.0%) and placebo groups (14.9 ± 11.5%; p = 0.616). Peak and area under the creatine kinase curve did not differ between both groups. LV ejection fraction by CMR was 51.0 ± 10.9% in the metoprolol group and 51.6 ± 10.8% in the placebo group (p = 0.68). The incidence of malignant arrhythmias was 3.6% in the metoprolol group versus 6.9% in placebo (p = 0.050). The incidence of adverse events was not different between groups. In a nonrestricted STEMI population, early intravenous metoprolol before PPCI was not associated with a reduction in infarct size. Metoprolol reduced the incidence of malignant arrhythmias in the acute phase and was not associated with an increase in adverse events.

Association of myocardial T1-mapping CMR with hemodynamics and RV performance in pulmonary hypertension

Early detection of right ventricular (RV) involvement in chronic pulmonary hypertension (PH) is essential due to prognostic implications. T1 mapping by cardiac magnetic resonance (CMR) has emerged as a noninvasive technique for extracellular volume fraction (ECV) quantification. We assessed the association of myocardial native T1 time and equilibrium contrast ECV (Eq-ECV) at the RV insertion points with pulmonary hemodynamics and RV performance in an experimental model of chronic PH. Right heart catheterization followed by immediate CMR was performed on 38 pigs with chronic PH (generated by surgical pulmonary vein banding) and 6 sham-operated controls. Native T1 and Eq-ECV values at the RV insertion points were both significantly higher in banded animals than in controls and showed significant correlation with pulmonary hemodynamics, RV arterial coupling, and RV performance. Eq-ECV values also increased before overt RV systolic dysfunction, offering potential for the early detection of myocardial involvement in chronic PH.

Efficacy and safety of out-of-hospital intravenous metoprolol administration in anterior ST-segment elevation acute myocardial infarction: insights from the METOCARD-CNIC trial

We seek to examine the efficacy and safety of prereperfusion emergency medical services (EMS)–administered intravenous metoprolol in anterior ST-segment elevation myocardial infarction patients undergoing eventual primary angioplasty. This is a prespecified subgroup analysis of the Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction trial population, who all eventually received oral metoprolol within 12 to 24 hours. We studied patients receiving intravenous metoprolol by EMS and compared them with others treated by EMS but not receiving intravenous metoprolol. Outcomes included infarct size and left ventricular ejection fraction on cardiac magnetic resonance imaging at 1 week, and safety by measuring the incidence of the predefined combined endpoint (composite of death, malignant ventricular arrhythmias, advanced atrioventricular block, cardiogenic shock, or reinfarction) within the first 24 hours. From the total population of the trial (N=270), 147 patients (54%) were recruited during out-of-hospital assistance and transferred to the primary angioplasty center (74 intravenous metoprolol and 73 controls). Infarct size was smaller in patients receiving intravenous metoprolol compared with controls (23.4 [SD 15.0] versus 34.0 [SD 23.7] g; adjusted difference –11.4; 95% confidence interval [CI] –18.6 to –4.3). Left ventricular ejection fraction was higher in the intravenous metoprolol group (48.1% [SD 8.4%] versus 43.1% [SD 10.2%]; adjusted difference 5.0; 95% CI 1.6 to 8.4). Metoprolol administration did not increase the incidence of the prespecified safety combined endpoint: 6.8% versus 17.8% in controls (risk difference –11.1; 95% CI –21.5 to –0.6). Out-of-hospital administration of intravenous metoprolol by EMS within 4.5 hours of symptom onset in our subjects reduced infarct size and improved left ventricular ejection fraction with no excess of adverse events during the first 24 hours.

Very low risk ST-segment elevation myocardial infarction? It exists and may be easily identified

Early discharge protocols have been proposed for ST-segment elevation myocardial infarction (STEMI) low risk patients despite the existence of few but significant cardiovascular events during mid-term follow-up. We aimed to identify a subgroup of patients among those considered low-risk in which prognosis would be particularly good. We analyzed 30-day outcomes and long-term follow-up among 1.111 STEMI patients treated with reperfusion therapy. Multivariate analysis identified seven variables as predictors of 30-day outcomes: Femoral approach; age > 65; systolic dysfunction; postprocedural TIMI flow < 3; elevated creatinine level > 1.5 mg/dL; stenosis of left-main coronary artery; and two or higher Killip class (FASTEST). A total of 228 patients (20.5%), defined as very low-risk (VLR), had none of these variables on admission. VLR group of patients compared to non-VLR patients had lower in-hospital (0% vs. 5.9%; p < 0.001) and 30-day mortality (0% vs. 6.25%: p < 0.001). They also presented fewer in-hospital complications (6.6% vs. 39.7%; p < 0.001) and 30-day major adverse events (0.9% vs. 4.5%; p = 0.01). Significant mortality differences during a mean follow-up of 23.8 ± 19.4 months were also observed (2.2% vs. 15.2%; p < 0.001). The first VLR subject died 11 months after hospital discharge. No cardiovascular deaths were identified in this subgroup of patients during follow-up. About a fifth of STEMI patients have VLR and can be easily identified. They have an excellent prognosis suggesting that 24–48 h in-hospital stay could be a feasible alternative in these patients.

Melatonin for cardioprotection in ST elevation myocardial infarction: Are we ready for the challenge?

Melatonin, an endocrine product of the pineal gland, is formed predominantly during the nighttime. Light has an inhibitory effect on pineal melatonin secretion. Pineal melatonin release is synchronised by this daily light-dark cycle via a multisynaptic pathway between the eyes and the pineal gland. Light stimulates the retina to modulate the activity of the suprachiasmatic nucleus, the master biological clock.1 The suprachiasmatic nucleus controls pineal melatonin synthesis and the concentrations of melatonin in the sera of healthy subjects, which reach values of 10−10 to 10−9 mol/L during the night, with much lower concentrations being present during the day. Many publications have shown that melatonin has an important role in a variety of cardiovascular pathophysiologic processes: the indoleamine has anti-inflammatory, antioxidant, antihypertensive, antithrombotic and antilipaemic properties.

Rat Atrial Responses To Bothrops Jararacussu (jararacuçu) Snake Venom.

Envenoming by the pitviper Bothrops jararacussu produces cardiovascular alterations, including coagulopathy, systemic hemorrhage, hypotension, circulatory shock and renal failure. In this work, we examined the activity of this venom in rat isolated right atria. Incubation with venom (0.025, 0.05, 0.1 and 0.2mg/ml) caused concentration-dependent muscle contracture that was not reversed by washing. Muscle damage was seen histologically and confirmed by quantification of creatine kinase-MB (CK-MB) release. Heating and preincubation of venom with p-bromophenacyl bromide (a phospholipase A2 inhibitor) abolished the venom-induced contracture and muscle damage. In contrast, indomethacin, a non-selective inhibitor of cyclooxygenase, and verapamil, a voltage-gated Ca(2+) channel blocker, did not affect the responses to venom. Preincubation of venom with Bothrops or Bothrops/Crotalus antivenom or the addition of antivenom soon after venom attenuated the venom-induced changes in atrial function and tissue damage. These results indicate that B. jararacussu venom adversely affected rat atrial contractile activity and muscle organization through the action of venom PLA2; these venom-induced alterations were attenuated by antivenom.

Rapidly Switching Multidirectional Defibrillation: Reversal Of Ventricular Fibrillation With Lower Energy Shocks.

Cardiac arrest after open surgery has an incidence of approximately 3%, of which more than 50% of the cases are due to ventricular fibrillation. Electrical defibrillation is the most effective therapy for terminating cardiac arrhythmias associated with unstable hemodynamics. The excitation threshold of myocardial microstructures is lower when external electrical fields are applied in the longitudinal direction with respect to the major axis of cells. However, in the heart, cell bundles are disposed in several directions. Improved myocardial excitation and defibrillation have been achieved by applying shocks in multiple directions via intracardiac leads, but the results are controversial when the electrodes are not located within the cardiac chambers. This study was designed to test whether rapidly switching shock delivery in 3 directions could increase the efficiency of direct defibrillation. A multidirectional defibrillator and paddles bearing 3 electrodes each were developed and used in vivo for the reversal of electrically induced ventricular fibrillation in an anesthetized open-chest swine model. Direct defibrillation was performed by unidirectional and multidirectional shocks applied in an alternating fashion. Survival analysis was used to estimate the relationship between the probability of defibrillation and the shock energy. Compared with shock delivery in a single direction in the same animal population, the shock energy required for multidirectional defibrillation was 20% to 30% lower (P < .05) within a wide range of success probabilities. Rapidly switching multidirectional shock delivery required lower shock energy for ventricular fibrillation termination and may be a safer alternative for restoring cardiac sinus rhythm.

Cardioprotective Mechanism Of S-nitroso-n-acetylcysteine Via S-nitrosated Betadrenoceptor-2 In The Ldlr-/- Mice.

Previous studies from our group have demonstrated the protective effect of S-nitroso-N-acetylcysteine (SNAC) on the cardiovascular system in dyslipidemic LDLr-/- mice that develop atheroma and left ventricular hypertrophy after 15 days on a high fat diet. We have shown that SNAC treatment attenuates plaque development via the suppression of vascular oxidative stress and protects the heart from structural and functional myocardial alterations, such as heart arrhythmia, by reducing cardiomyocyte sensitivity to catecholamines. Here we investigate the ability of SNAC to modulate oxidative stress and cell survival in cardiomyocytes during remodeling and correlation with β₂-AR signaling in mediating this protection. Ventricular superoxide (O₂⁻) and hydrogen peroxide (H₂O₂) generation was measured by HPLC methods to allow quantification of dihydroethidium (DHE) products. Ventricular histological sections were stained using terminal dUTP nick-end labeling (TUNEL) to identify nuclei with DNA degradation (apoptosis) and this was confirmed by Western blot for cleaved caspase-3 and caspase-7 protein expression. The findings show that O₂⁻ and H₂O₂ production and also cell apoptosis were increased during left ventricular hypertrophy (LVH). SNAC treatment reduced oxidative stress during on cardiac remodeling, measured by decreased H₂O₂ and O₂⁻ production (65% and 52%, respectively), and a decrease in the ratio of p-Ser1177 eNOS/total eNOS. Left ventricle (LV) from SNAC-treated mice revealed a 4-fold increase in β₂-AR expression associated with coupling change to Gi; β₂-ARs-S-nitrosation (β₂-AR-SNO) increased 61%, while apoptosis decreased by 70%. These results suggest that the cardio-protective effect of SNAC treatment is primarily through its anti-oxidant role and is associated with β₂-ARs overexpression and β₂-AR-SNO via an anti-apoptotic pathway.

Diagnostic agreement between panoramic radiographs and color doppler images of carotid atheroma

The aim of this study was to investigate the agreement between diagnoses of calcified atheroma seen on panoramic radiographs and color Doppler images. Our interest stems from the fact that panoramic images can show the presence of atheroma regardless of the level of obstruction detected by color Doppler images. Panoramic and color Doppler images of 16 patients obtained from the archives of the Health Department of the city of Valença, RJ, Brazil, were analyzed in this study. Both sides of each patient were observed on the images, with a total of 32 analyzed cervical regions. The level of agreement between diagnoses was analyzed using the Kappa statistics. There was a high level of agreement, with a Kappa value of 0.78. In conclusion, panoramic radiographs can help detecting calcifications in the cervical region of patients susceptible to vascular diseases predisposing to myocardial infarction and cerebrovascular accidents. If properly trained and informed, dentists can refer their patients to a physician for a cardiovascular evaluation in order to receive proper and timely medical treatment.

Uso de suporte hemodinâmico e respiratório por meio de oxigenação extracorpórea por membrana (ECMO) venoarterial em um paciente politraumatizado

Existem poucos relatos na literatura sobre o uso de oxigenação extracorpórea por membrana venoarterial por dupla disfunção decorrente de contusão cardíaca e pulmonar no paciente politraumatizado. Relatamos o caso de um paciente de 48 anos, vítima de acidente de motocicleta e automóvel, que evoluiu rapidamente com choque refratário com baixo débito cardíaco por contusão miocárdica e hipoxemia refratária decorrente de contusão pulmonar, tórax instável e pneumotórax bilateral. O suporte extracorpóreo foi uma medida efetiva de resgate para esse caso dramático, e o seu uso pôde ser interrompido com sucesso no 4º dia após o trauma. O paciente evoluiu com extenso infarto cerebral, morrendo no 7º dia de internação

Sildenafil preserves diastolic relaxation after reduction by L-NAME and increases phosphodiesterase-5 in the intercalated discs of cardiac myocytes and arterioles

OBJECTIVES: We investigated the influence of sildenafil on cardiac contractility and diastolic relaxation and examined the distribution of phosphodiesterase-5 in the hearts of hypertensive rats that were treated with by NG-nitro-L-arginine methyl ester (L-NAME). METHODS: Male Wistar rats were treated with L-NAME and/or sildenafil for eight weeks. The Langendorff method was used to examine the effects of sildenafil on cardiac contractility and diastolic relaxation. The presence and location of phosphodiesterase-5 and phosphodiesterase-3 were assessed by immunohistochemistry, and cGMP plasma levels were measured by ELISA. RESULTS: In isolated hearts, sildenafil prevented the reduction of diastolic relaxation (dP/dt) that was induced by L-NAME. In addition, phosphodiesterase-5 immunoreactivity was localized in the intercalated discs between the myocardial cells. The staining intensity was reduced by L-NAME, and sildenafil treatment abolished this reduction. Consistent with these results, the plasma levels of cGMP were decreased in the L-NAME-treated rats but not in rats that were treated with L-NAME + sildenafil. CONCLUSION: The sildenafil-induced attenuation of the deleterious hemodynamic and cardiac morphological effects of L-NAME in cardiac myocytes is mediated (at least in part) by the inhibition of phosphodiesterase-5.