Long-term use of carvedilol in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention.

BACKGROUND: Despite its recommendation by the current guidelines, the role of long-term oral beta-blocker therapy has never been evaluated by randomized trials in uncomplicated ST-segment elevation myocardial infarction (STEMI) patients without heart failure, left ventricular dysfunction or ventricular arrhythmia who underwent primary percutaneous coronary intervention (PCI). METHODS AND RESULTS: In a multi-center, open-label, randomized controlled trial, STEMI patients with successful primary PCI within 24 hours from the onset and with left ventricular ejection fraction (LVEF) ≥40% were randomly assigned in a 1-to-1 fashion either to the carvedilol group or to the no beta-blocker group within 7 days after primary PCI. The primary endpoint is a composite of all-cause death, myocardial infarction, hospitalization for heart failure, and hospitalization for acute coronary syndrome. Between August 2010 and May 2014, 801 patients were randomly assigned to the carvedilol group (N = 399) or the no beta-blocker group (N = 402) at 67 centers in Japan. The carvedilol dose was up-titrated from 3.4±2.1 mg at baseline to 6.3±4.3 mg at 1-year. During median follow-up of 3.9 years with 96.4% follow-up, the cumulative 3-year incidences of both the primary endpoint and any coronary revascularization were not significantly different between the carvedilol and no beta-blocker groups (6.8% and 7.9%, P = 0.20, and 20.3% and 17.7%, P = 0.65, respectively). There also was no significant difference in LVEF at 1-year between the 2 groups (60.9±8.4% and 59.6±8.8%, P = 0.06). CONCLUSION: Long-term carvedilol therapy added on the contemporary evidence-based medications did not seem beneficial in selected STEMI patients treated with primary PCI. TRIAL REGISTRATION: CAPITAL-RCT (Carvedilol Post-Intervention Long-Term Administration in Large-scale Randomized Controlled Trial) ClinicalTrials.gov.number, NCT 01155635.

Comparison of Frequency and Characteristics of Patients With Atrial Fibrillation Having Ablation With Versus Without Coronary Narrowing (≥50%) by Angiography.

Atrial fibrillation (AF) shares background comorbidities with coronary artery disease (CAD), including hypertension and diabetes mellitus. The aim of the study is to evaluate the prevalence, risk factors, and prognostic significance of CAD among patients who underwent catheter ablation for AF. In 544 consecutive registered patients who underwent catheter ablation for AF (CHADS2 score 1.2 ± 1.1, paroxysmal AF 57%), quantitative coronary angiography was used to detect CAD, defined as luminal narrowing of ≥50% in diameter. Univariate and multiple logistic regression analyses were applied to evaluate the risk factors of CAD. Subsequent clinical events up to 1 year were obtained in all the patients. CAD was found in 70 patients (13%). The factors associated with the presence of CAD in AF patients who underwent catheter ablation were similar to traditional coronary risk factors such as hypertension and diabetes mellitus. AF patients with CAD had a higher CHADS2 score than those without CAD (1.5 ± 1.1 vs 1.1 ± 1.0, p = 0.009). Hence, a CHADS2 score ≥1 may be an alternative risk factor to predict CAD. Previous coronary revascularization (14% with CAD vs 6% without CAD) and paroxysmal AF (69% vs 55%) were also associated with CAD. During follow-up, patients with CAD experienced acute coronary syndrome (n = 2) and coronary revascularization (n = 18); no such events were recorded in those without CAD. In addition to traditional risk factors, CHADS2 score, previous revascularization, and paroxysmal AF may be new risk factors for CAD in AF patients.

Impact of basal inferolateral scar burden determined by automatic analysis of 99mTc-MIBI myocardial perfusion SPECT on the long-term prognosis of cardiac resynchronization therapy.

AIMS: Left-ventricular (LV) scarring may be associated with a poor response to cardiac resynchronization therapy (CRT). The automatic analysis of myocardial perfusion single-photon emission computed tomography (MP-SPECT) may provide objective quantification of LV scarring. We investigated the impact of LV scarring determined by an automatic analysis of MP-SPECT on short-term LV volume response as well as long-term outcome. METHODS AND RESULTS: We studied consecutive 51 patients who were eligible to undergo 99mTc-MIBI MP-SPECT both at baseline and 6 months after CRT (ischaemic cardiomyopathies 31%). Quantitative perfusion SPECT was used to evaluate the defect extent (an index of global scarring) and the LV 17-segment regional uptake ratio (an inverse index of regional scar burden). The primary outcome was the composite of overall mortality or first hospitalization for worsening heart failure. A high global scar burden and a low mid/basal inferolateral regional uptake ratio were associated with volume non-responders to CRT at 6 months. The basal inferolateral regional uptake ratio remained as a predictor of volume non-response after adjusting for the type of cardiomyopathy. During a median follow-up of 36.1 months, the outcome occurred in 28 patients. The patients with a low basal inferolateral regional uptake ratio with a cutoff value of 57% showed poor prognosis (log-rank P= 0.006). CONCLUSION: The scarring determined by automatic analysis of MP-SPECT images may predict a poor response to CRT regardless of the pathogenesis of cardiomyopathy. The basal inferolateral scar burden in particular may have an adverse impact on long-term prognosis.

Non-vitamin K antagonist oral anticoagulants versus warfarin for cardioversion of atrial fibrillation in clinical practice: A single-center experience.

BACKGROUND: Anticoagulation therapy with the vitamin K antagonist (VKA) warfarin has been demonstrated to reduce thromboembolic risk after electrical cardioversion (ECV). However, data concerning ECV with non-VKA oral anticoagulants (NOACs) is limited. The objective of this study was to determine the efficacy and safety of NOACs in patients undergoing ECV in a real-world clinical practice at a single center in Japan. METHODS: We retrospectively analyzed the data of 406 consecutive patients who underwent ECV for atrial fibrillation (AF) or flutter under anticoagulation with one of the three NOACs (n=149) or with a VKA (n=257). RESULTS: The CHADS2 and HAS-BLED scores were significantly higher in the VKA group, whereas the NOACs group had a tendency toward greater spontaneous echo contrast grades. After ECV, ischemic stroke occurred in three patients of the VKA group and one patient in the NOAC group, all of whom had persistent AF, indicating no significant difference in the thromboembolic event rate within 30 days following ECV. No other thromboembolic events, major bleeding, or death occurred in either group. Among the NOAC and VKA patients in whom we newly introduced an oral anticoagulant to perform ECV, the number of days leading to ECV was significantly lesser for the NOAC patients. CONCLUSION: NOACs may be used as an alternative to VKAs for ECV and may allow prompt ECV in clinical practices.

Evaluation of the safety and efficacy of TY-51924 in patients with ST elevated acute myocardial infarction - Early phase II first in patient pilot study.

BACKGROUND: In myocardial ischemia-reperfusion injuries, the involvement of the Na(+)/H(+) exchanger (NHE) is considered to be one of the pathogenic mechanisms following reperfusion. TY-51924 is a novel hydrophilic NHE inhibitor with a lower risk of central neurotoxicity than previous NHE inhibitors. This open-label, dose-escalating study was undertaken to investigate the safety, efficacy, and pharmacokinetics of TY-51924 in patients with ST-elevation myocardial infarction (STEMI). METHODS: Consent was obtained from a total of 30 patients with first anterior STEMI. After 12 patients were determined to be ineligible, the remaining 18 patients, each of whom was undergoing primary percutaneous coronary intervention (pPCI), received TY-51924 intravenously up to 10, 20, or 30mg/kg as the low-, medium-, or high-dose groups, respectively (n=6 in each group). The primary endpoints were safety (up to 7 days) and plasma drug concentration. The myocardial salvage index (MSI) was measured by (201)Tl/(123)I-beta-methyl-p-iodophenyl pentadecanoic acid single photon emission computed tomography (SPECT) 3-5 days after pPCI. RESULTS: No side effects were observed. Plasma drug concentrations increased dose-dependently, and were subsequently eliminated rapidly. MSIs were 0.118, 0.335, and 0.192 in the low-, medium-, and high-dose groups, respectively. In additional analysis, the combined MSIs in the medium- and high-dose groups were significantly higher than those in the low-dose group, in patients with a longer time from symptom onset to reperfusion (p=0.0247). CONCLUSIONS: No side effects were observed even at the highest dose with this novel hydrophilic NHE inhibitor. Therefore, TY-51924 is thought to be safe in patients with STEMI, even at the highest dose. Potential cardioprotective effects of intravenous TY-51924 might be expected based on the results obtained for the MSIs using SPECT at 20-30mg/kg. However, further large-scale, double-blind, placebo-controlled clinical studies are required to confirm the efficacy and safety implied in the current study.

Randomized controlled trial of TY-51924, a novel hydrophilic NHE inhibitor, in acute myocardial infarction.

BACKGROUND: In patients with ST-elevation acute myocardial infarction (STEMI), reperfusion therapy limits infarct size, but can directly evoke myocardial reperfusion injury. Activation of the Na(+)/H(+) exchanger (NHE) plays an important role in reperfusion injury. TY-51924, a novel NHE inhibitor, significantly reduced infarct size in animal studies and was well tolerated in early-phase clinical trials. This study aim was to evaluate the efficacy and safety of TY-51924 in patients with STEMI. METHODS: In this multicenter, randomized, double-blind, placebo-controlled Phase II trial, 105 patients with first anterior STEMI undergoing primary percutaneous coronary intervention (pPCI) were randomly assigned to receive an intravenous infusion of either TY-51924 or placebo. Primary endpoints were myocardial salvage index (MSI) as determined by single photon emission computed tomography (SPECT) 3-5 days after pPCI and safety up to 7 days. RESULTS: Baseline characteristics were similar in the two groups. MSI 3-5 days after pPCI (0.200 vs. 0.290, p=0.56), 3 months after pPCI (0.470 vs. 0.500, p=0.76), and the incidences of side effects did not differ between the two groups as a whole. However, on post hoc analysis of 52 patients with a large area at risk (AAR) (≥38%) and no antegrade coronary flow, MSI by SPECT at 3 months after pPCI was significantly higher in TY-51924 group (0.450 vs. 0.320, p=0.03). TY-51924 did not adversely influence hemodynamics. CONCLUSIONS: TY-51924 did not improve MSI or increase side effects as a whole. However, TY-51924 is potentially cardioprotective in the presence of a large AAR and no antegrade coronary flow.

Application of the newly developed Japanese adenosine normal database for adenosine stress myocardial scintigraphy.

OBJECTIVES: The currently available Japanese normal database (NDB) in stress myocardial perfusion scintigraphy recommended by the Japanese Society of Nuclear Medicine (JSNM-NDB) is created based on the data from exercise tests. The newly developed adenosine normal database (ADS-NDB) remains to be validated for patients undergoing adenosine stress test. We tested whether the diagnostic accuracy of adenosine stress test is improved by the use of ADS-NDB (Kanazawa University). METHODS: Of 233 consecutive patients undergoing (99m)Tc-MIBI adenosine stress test, 112 patients were tested. The stress/rest myocardial (99m)Tc-MIBI single-photon emission computed tomography (SPECT) images were analyzed by AutoQUANT 7.2 with both ADS-NDB and JSNM-NDB. The summed stress score (SSS) and summed difference score (SDS) were calculated. The agreements of the post-stress defect severity between ADS-NDB and JSNM-NDB were assessed using a weighted kappa statistic. RESULTS: In all patients, mean SSSs of all, right coronary artery (RCA), left anterior descending (LAD), and left circumflex (LCx) territories were significantly lower with ADS-NDB than those with JSNM-NDB. Mean SDSs in all, RCA, and LAD territories were significantly lower with ADS-NDB than those with JSNM-NDB. In 28 patients with significant coronary stenosis, the mean SSS in the RCA territory was significantly lower with ADS-NDB than that with JSNM-NDB. In 84 patients without ischemia, both mean SSSs and SDSs in all, RCA, LAD, and LCx territories were significantly lower with ADS-NDB than those with JSNM-NDB. Weighted kappa values of all patients, patients with significant stenosis, and patients without ischemia were 0.89, 0.83, and 0.92, respectively. CONCLUSIONS: Differences were observed between results from ADS-NDB and JSNM-NDB. The diagnostic accuracy of adenosine stress myocardial perfusion scintigraphy may be improved by reducing false-positive results.

Antiplatelet therapy discontinuation and stent thrombosis after sirolimus-eluting stent implantation: five-year outcome of the j-Cypher Registry.

BACKGROUND: The influence of antiplatelet therapy discontinuation on the incidence of stent thrombosis, especially very late stent thrombosis, after drug-eluting stent implantation has not been yet fully addressed. METHODS: Relationship between antiplatelet therapy discontinuation and stent thrombosis up to 5years was evaluated in 12,812 consecutive patients undergoing sirolimus-eluting stents (SES) implantation in the j-Cypher registry. Data on status of antiplatelet therapy during follow-up were collected prospectively. RESULTS: Median follow-up interval was 1699days (interquartile range, 1184-1928days). Incidences of definite stent thrombosis were 0.34% at 30days, 0.55% at 1year, and 1.6% at 5years. Dual antiplatelet therapy was maintained in 97.4%, 63%, and 43.9% of patients at 30days, 1year, and 5years, respectively. The rates of stent thrombosis in patients who discontinued both thienopyridine and aspirin were significantly higher in the time intervals of 31-365days, 2-3years and 3-4years, and tended to be higher in the time intervals of 1-2years and 4-5years than those in patients who continued both (31-365days: 1.26% versus 0.2%, P<0.001; 1-2years: 0.59% versus 0.15%, P=0.06; 2-3years: 1.35% versus 0.2%, P=0.004; 3-4years: 1.09% versus 0.25%, P=0.0496; 4-5years: 1.35% versus 0.43%, P=0.17). Patients who discontinued either thienopyridine or aspirin only did not have an excess of stent thrombosis in any time intervals. CONCLUSIONS: In conclusion, discontinuation of both thienopyridine and aspirin, but not discontinuation of thienopyridine or aspirin only, was associated with an increased incidence of late and very late stent thrombosis up to 5years after SES implantation.

Left ventricular dyssynchrony in patients with moderate coronary stenosis and border line fractional flow reserve.

The cutoff values of fractional flow reserve (FFR) to detect physiological myocardial ischemia are still controversial. Some studies have reported that left ventricular (LV) dyssynchrony occurs in patients with coronary artery disease (CAD). The purpose of this study was to investigate LV dyssynchrony in patients with moderate coronary stenosis and borderline FFR, using stress electrocardiographically-gated myocardial perfusion single-photon emission computed tomography (SPECT). The study population comprised 10 patients with moderate (50-75% diameter) stenosis and an FFR in the range 0.75-0.90, who were compared to 10 control subjects. All underwent stress myocardial (99m)Tc-sestamibi (MIBI) or tetrofosmin SPECT imaging. The regional time to end systole (TES), time to peak ejection (TPE), and time to peak filling (TPF) were obtained as indexes of perfusion and function, using gated SPECT (pFAST) in combination with Cardio Gated SPECT Regional Assessment for LV Function (cardioGRAF). The dyssynchrony index (DI) was also calculated. The DI of post-stress TES was significantly greater than that of rest in patients with moderate CAD (4.8 ± 2.8 vs. 2.7 ± 1.5, P = 0.01), but there were no significant differences in the control subjects (3.0 ± 1.7 vs. 2.9 ± 1.9, P = 0.99). There were no significant differences in TPE and TPF between the groups. In conclusion, LV dyssynchrony may occur after stress in patients with coronary stenosis and borderline FFR, even without a significant reduction in perfusion.

Presence of myocardial hypoenhancement on multidetector computed tomography after primary percutaneous coronary intervention in acute myocardial infarction predicts poor prognosis.

BACKGROUND: Recent research has suggested that patients with greater delayed contrast-enhanced size by multidetector computed tomography (MDCT) are more likely to experience adverse cardiac events and have poor prognoses over the long term. The myocardial hypoenhancement area in the delayed contrast-enhanced effect suggests microvascular obstruction. The outcomes of patients with a hypoenhancement area detected by MDCT have not been clear. We examined the clinical importance of myocardial hypoenhancement detected by delayed contrast-enhanced MDCT after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction. METHODS AND RESULTS: In 80 patients with acute myocardial infarction, MDCT was performed immediately after primary PCI. We investigated the outcomes of the patients with hypoenhancement detected by MDCT. Myocardial hypoenhancement was observed in 14 patients (17.5%). All 14 of these patients with hypoenhancement had a transmural infarction, and their infarct volume was significantly higher than those of the patients without hypoenhancement (n=66). During the median follow-up period of 309 days, the appearance of myocardial hypoenhancement was associated with the presence of slow flow/no-reflow, time from onset to reperfusion ≥6 h, aging, smoking, chronic kidney disease, and hyper-low-density lipoprotein cholesterolemia. The incidence of major adverse cardiovascular events (MACE) was significantly higher in the patients with hypoenhancement compared to those without hypoenhancement, regardless of the myocardial infarct volume. CONCLUSIONS: These results indicate that the presence of myocardial hypoenhancement in delayed contrast-enhanced MDCT after PCI as well as the extent of infarct area is an important predictor of MACE.

Omentin prevents myocardial ischemic injury through AMP-activated protein kinase- and Akt-dependent mechanisms.

OBJECTIVES: This study examined the impact of omentin on myocardial injury in a mouse model of ischemia/reperfusion (I/R) and explored its underlying mechanisms. BACKGROUND: Obesity is a major risk factor for ischemic heart disease. Omentin is a circulating adipokine that is down-regulated by obesity. METHODS: In patients who underwent successful reperfusion treatment after acute myocardial infarction, cardiac function and perfusion defect were assessed by using scintigraphic images. Mice were subjected to myocardial ischemia followed by reperfusion. RESULTS: This study found that high levels of plasma omentin were associated with improvement of heart damage and function after reperfusion therapy in patients with acute myocardial infarction. Systemic administration of human omentin to mice led to a reduction in myocardial infarct size and apoptosis after I/R, which was accompanied by enhanced phosphorylation of AMP-activated protein kinase (AMPK) and Akt in the ischemic heart. Fat-specific overexpression of human omentin also resulted in reduction of infarct size after I/R. Blockade of AMPK or Akt activity reversed omentin-induced inhibition of myocardial ischemic damage and apoptosis in mice. In cultured cardiomyocytes, omentin suppressed hypoxia/reoxygenation-induced apoptosis, which was blocked by inactivation of AMPK or Akt. CONCLUSIONS: Our data indicate that omentin functions as an adipokine that ameliorates acute ischemic injury in the heart by suppressing myocyte apoptosis through both AMPK- and Akt-dependent mechanisms.

Identification of a glutamic acid repeat polymorphism of ALMS1 as a novel genetic risk marker for early-onset myocardial infarction by genome-wide linkage analysis.

BACKGROUND: Myocardial infarction (MI) is a leading cause of death worldwide. Given that a family history is an independent risk factor for coronary artery disease, genetic variants are thought to contribute directly to the development of this condition. The identification of susceptibility genes for coronary artery disease or MI may thus help to identify high-risk individuals and offer the opportunity for disease prevention. METHODS AND RESULTS: We designed a 5-step protocol, consisting of a genome-wide linkage study followed by association analysis, to identify novel genetic variants that confer susceptibility to coronary artery disease or MI. A genome-wide affected sib-pair linkage study with 221 Japanese families with coronary artery disease yielded a statistically significant logarithm of the odds score of 3.44 for chromosome 2p13 and MI. Further association analysis implicated Alström syndrome 1 gene (ALMS1) as a candidate gene within the linkage region. Validation association analysis revealed that representative single-nucleotide polymorphisms of the ALMS1 promoter region were significantly associated with early-onset MI in both Japanese and Korean populations. Moreover, direct sequencing of the ALMS1 coding region identified a glutamic acid repeat polymorphism in exon 1, which was subsequently found to be associated with early-onset MI. CONCLUSIONS: The glutamic acid repeat polymorphism of ALMS1 identified in the present study may provide insight into the pathogenesis of early-onset MI.

Comparison of 5-year outcomes in patients with and without unprotected left main coronary artery disease after treatment with sirolimus-eluting stents: insights from the j-Cypher registry.

OBJECTIVES: This study assessed 5-year outcomes after implantation of sirolimus-eluting stents (SES) for unprotected left main coronary artery (ULMCA) disease in comparison with that for non-left main disease. BACKGROUND: More information on long-term outcomes after ULMCA stenting is needed. METHODS: The j-Cypher is a multicenter prospective registry of consecutive patients undergoing SES implantation in Japan. RESULTS: Among 12,812 patients enrolled in the j-Cypher registry, the unadjusted mortality rate at 5 years was significantly higher in patients with ULMCA stenting than in patients without ULMCA stenting (22.8% vs. 14.1%; p < 0.0001); however, the risk for death with ULMCA stenting was no longer significant after adjusting for confounders (hazard ratio: 1.18, 95% confidence interval: 0.95 to 1.46; p = 0.14). In the lesion-level comparison, the nonbifurcation ULMCA lesions treated exclusively with SES had a significantly lower rate of target lesion revascularization (TLR) than those in non-ULMCA nonbifurcation lesions (2.4% vs. 12.7%; p = 0.04). Among bifurcation lesions, those treated with a provisional 2-stent approach had similar rates of TLR (12.1% vs. 11.4%; p = 0.79) between the ULMCA and non-ULMCA groups. Lesions treated with an elective 2-stent approach had higher TLR rates in the ULMCA group as compared with the non-ULMCA group (33.5% vs. 19.7%; p = 0.002). CONCLUSIONS: The safety of ULMCA stenting relative to non-LMCA stenting was maintained through 5 years follow-up. In terms of efficacy, SES implantation in nonbifurcation ULMCA lesions was associated with an extremely low cumulative incidence of TLR, whereas the elective 2-stent approach for ULMCA bifurcation lesions was associated with a markedly higher cumulative incidence of TLR as compared with that for non-ULMCA bifurcation lesions.

Impact of angiotensin II receptor blocker therapy (olmesartan or valsartan) on coronary atherosclerotic plaque volume measured by intravascular ultrasound in patients with stable angina pectoris.

Coronary plaques can be reduced by some medications. The aim of this study was to compare the effects of 2 angiotensin II receptor blockers (olmesartan at 20 mg/day or valsartan at 80 mg/day) on coronary plaque by coronary intravascular ultrasound. One hundred hypertensive patients with stable angina pectoris who underwent elective percutaneous coronary intervention were randomly selected to receive 1 of the 2 angiotensin II receptor blockers after coronary intervention. Nontarget coronary lesions with mild to moderate stenosis were measured by volumetric intravascular ultrasound at baseline and after 6 months. After 6 months, both the olmesartan and the valsartan groups showed significant reduction of the examined coronary plaque volume (46.2 ± 24.1 mm³ at baseline vs 41.6 ± 21.1 mm³ at 6 months: 4.7% decrease, p = 0.0002; and 47.2 ± 32.7 mm³ at baseline vs 42.5 ± 30.2 mm³ at 6 months: 4.8% decrease, p = 0.002, respectively). There was no statistically significant difference of plaque regression between the 2 groups (p = 0.96). In conclusion, there was a significant decrease from baseline in the coronary plaque volume in patients with stable angina pectoris who received olmesartan or valsartan for 6 months. In addition, there was no significant difference in the reduction of plaque volume achieved by these 2 medications.

Rescue pulmonary vein isolation for hemodynamically unstable atrial fibrillation storm in a patient with an acute extensive myocardial infarction.

BACKGROUND: New-onset atrial fibrillation in patients hospitalized for an acute myocardial infarction often leads to hemodynamic deterioration and has serious adverse prognostic implications; mortality is particularly high in patients with congestive heart failure and/or a reduced left ventricular ejection fraction. The mechanism of atrial fibrillation in the context of an acute myocardial infarction has not been well characterized and an effective treatment other than optimal medical therapy and mechanical hemodynamic support are expected. CASE PRESENTATION: A 71 year-old male with an acute myocardial infarction due to an occlusion of the left main coronary artery was treated with percutaneous coronary intervention. He had developed severe congestive heart failure with a left ventricular ejection fraction of 34%. The systemic circulation was maintained with an intraaortic balloon pump, continuous hemodiafiltration, and mechanical ventilation until atrial fibrillation occurred on day 3 which immediately led to cardiogenic shock. Because atrial fibrillation was refractory to intravenous amiodarone, beta-blockers, and a total of 15 electrical cardioversions, the patient underwent emergent radiofrequency catheter ablation on day 4. Soon after electrical cardioversion, ectopies from the right superior pulmonary vein triggered the initiation of atrial fibrillation. The right pulmonary veins were isolated during atrial fibrillation. Again, atrial fibrillation was electrically cardioverted, then, sinus rhythm was restored. Subsequently, the left pulmonary veins were isolated. The stabilization of the hemodynamics was successfully achieved with an increase in the blood pressure and urine volume. Hemodiafiltration and amiodarone were discontinued. The patient had been free from atrial fibrillation recurrence until he suddenly died due to ventricular fibrillation on day 9. CONCLUSIONS: To the best of our knowledge, this is the first report of pulmonary vein isolation for a rescue purpose applied in a patient with hemodymically unstable atrial fibrillation complicated with an acute myocardial infarction. This case demonstrates that ectopic activity in the pulmonary veins may be responsible for triggering atrial fibrillation in the critical setting of an acute myocardial infarction and thus pulmonary vein isolation could be an effective therapeutic option.