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Objective: Heme oxygenase-1 (HO-1) degrades heme to CO, iron, and biliverdin/bilirubin. Although serum bilirubin levels were often reported in patients with coronary artery disease (CAD), HO-1 levels in patients with CAD and the association between HO-1 and bilirubin levels have not been clarified., Methods: We measured plasma HO-1 and serum total bilirubin levels in 262 patients undergoing coronary angiography., Results: HO-1 levels were higher in patients with CAD than without CAD (median 0.46 vs. 0.35 ng/mL, P < 0.01), but bilirubin were lower in patients with CAD than without CAD (0.69 vs. 0.75 mg/dL, P < 0.02). Notably, HO-1 levels in CAD(-), 1-vessel, 2-vessel, and 3-vessel disease were 0.35, 0.51, 0.45, and 0.44 ng/mL, and were highest in 1-vessel disease (P < 0.05). Bilirubin levels in CAD(-), 1-vessel, 2-vessel, and 3-vessel disease were 0.75, 0.70, 0.68, and 0.66 mg/dL (P = NS). No correlation was found between HO-1 and bilirubin levels. In multivariate analysis, HO-1 levels were a significant factor for CAD independent of atherosclerotic risk factors and bilirulin levels. Odds ratio for CAD was 2.32 (95%CI = 1.29-4.17) for high HO-1 (>0.35 ng/mL)., Conclusions: Patients with CAD were found to have high HO-1 and low bilirubin levels in blood, but no correlation was found between HO-1 and bilirubin levels., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Background: Sestrin2 is a stress-inducible antioxidant protein that plays a protective role against oxidative stress. However, blood sestrin2 concentrations in subjects with carotid atherosclerosis have not been elucidated., Methods: We investigated plasma sestrin2 concentrations in 152 subjects undergoing carotid ultrasonography. Plaque severity was evaluated as plaque score., Results: Of the 152 subjects, plaque was found in 63 (41%). Plasma sestrin2 concentrations were higher in 63 subjects with plaque than in 89 without plaque (median 14.1 vs. 12.8 ng/ml, P < 0.02). A stepwise increase in sestrin2 concentrations was found depending on plaque score: 12.8 ng/ml in score = 0 (n = 89), 12.7 ng/ml in score = 1 (n = 31), and 15.9 ng/ml in score ≥2 (n = 32)(P < 0.005). Especially, sestrin2 concentrations in subjects with score ≥ 2 were higher than in score = 0 and score = 1 (P < 0.05). Sestrin2 concentrations correlated with plaque score (r = 0.24, P < 0.005). In multivariate analysis, sestrin2 concentration was an independent factor associated with score ≥ 2. Odds ratio for score ≥ 2 was 5.70 (95%CI = 1.99-16.35) for high sestrin2 concentration (>13.0 ng/ml)., Conclusion: Plasma sestrin2 concentrations were found to be high in subjects with carotid plaque and to be associated with plaque severity. High plasma sestrin2 concentrations in subjects with carotid plaque may reflect a protective response against the progression of carotid atherosclerosis., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Background: Bleeding complications remain one of the most important challenges in percutaneous coronary intervention (PCI), particularly in Asians who are known to be vulnerable to the use of antiplatelets or anticoagulants. However, the incidence and predictors of bleeding complications after PCI have not been thoroughly investigated in Japan., Methods: We studied 13,075 consecutive patients in a Japanese multicenter PCI registry (Japan Cardiovascular Database - Keio interhospital Cardiovascular Study: JCD-KiCS) from September 2008 to March 2014. Multivariate logistic regression analysis was performed to investigate independent predictors of bleeding complications, and to create three risk prediction models for bleeding events. Model 1 included patients' characteristics alone. In model 2, we added patients' clinical presentation. Model 3 included covariates in model 2 along with angiographic and technical factors. Model discrimination was assessed using the area under the receiver operating curve (AUC)., Results: Overall, bleeding complications, according to the pre-specified US National Cardiovascular Data Registry criteria, were observed in 402 patients (3.1%). Independent predictors of bleeding complications included age, female gender, previous PCI, previous heart failure, hemodialysis (variables included in model 1), ST-elevation and non-ST-elevation myocardial infarction, cardiogenic shock (added in model 2), transradial intervention, use of intra-aortic balloon pumping or a rotablator, and PCI for chronic total occlusion (added in model 3). Above all, previous PCI and transradial intervention were inverse predictors of bleeding. The predictability of the risk models improved as the number of variables increased, with AUC of 0.667, 0.747, and 0.791 for models 1, 2, and 3, respectively., Conclusions: The incidence of bleeding complications among Japanese PCI patients was approximately 3% in standard nomenclature, which is equivalent to that of other international registries. Patients' characteristics, clinical presentation, and angiographic and technical factors all independently contributed to its prediction., (Copyright © 2016 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Mitochondrial impairment and increased oxidative stress are considered to be involved in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease. Coenzyme Q10 (CoQ10) is a component of the electron transport chain localized on the inner membrane of the mitochondria. In addition to its bioenergetic activity required for ATP synthesis, CoQ10 also has antioxidant activity in mitochondrial and lipid membranes, which protects against the reactive oxidative species generated during oxidative phosphorylation. Several previous studies had reported no significant differences in serum CoQ10 levels between patients with and without dementia, such as Alzheimer's disease. However, in this issue of Atherosclerosis, Yamagishi et al. demonstrate for the first time that a lower serum CoQ10 level is associated with a greater risk of dementia in a Japanese general population. These findings suggest that assessing serum CoQ10 levels could be useful for predicting the development of dementia, rather than as a biomarker for the presence of dementia., (Copyright © 2014. Published by Elsevier Ireland Ltd.)

Apelin is an endogenous ligand for the orphan G protein-coupled receptor (APJ receptor). Apelin is predominantly expressed in endocardial and vascular endothelial cells, while APJ receptor is localized to endothelial and smooth muscle cells, and cardiomyocytes. Apelin has recently attracted much attention due to its promotive effects on angiogenesis and its protective effects against mycardial infarction. In this issue of Atherosclerosis, Akboga et al. investigated plasma apelin levels in patients with stable angina and severe coronary artery stenosis and provided the first evidence that higher plasma apelin levels are associated with better coronary collateral development, suggesting that apelin plays a role in coronary collateral development., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Objective: Although previous randomized clinical trials established a basis for lipid guidelines worldwide, they employed fixed doses of statins throughout trials (fire-and-forget approach). In the real clinical setting, however, statin doses are titrated to achieve target low-density lipoprotein cholesterol (LDL-C) levels (treat-to-target approach). The major objective was to investigate whether intensive lipid-lowering therapy using the treat-to-target approach yielded greater regression of aortic plaques., Methods: We therefore performed a prospective, randomized trial comparing the effects of standard (achieve LDL-C levels recommended by the Japanese guidelines) and intensive (achieve 30% lower LDL-C levels than standard) rosuvastatin therapy for 1 year in 60 hypercholesterolemic patients with a primary endpoint of aortic atherosclerotic plaques evaluated by non-invasive magnetic resonance imaging (MRI)., Results: Average doses were 2.9 ± 3.1 and 6.5 ± 5.1 mg/day for standard (n = 29) and intensive therapy group (n = 31), respectively. Although both therapies significantly reduced LDL-C and high-sensitivity C-reactive protein (hsCRP) levels, LDL-C reduction was significantly greater in the intensive group (-46 vs. -34%). MRI study showed that thoracic aortic plaques were significantly regressed in both groups, with greater regression of thoracic plaque in the intensive group (-9.1 vs. -3.2%, p = 0.01). Multivariate analyses revealed that thoracic plaque regression was significantly correlated with hsCRP reduction, but not with changes in serum lipids, endothelial function, or doses of rosuvastatin., Conclusion: Intensive statin therapy with titration targeting lower LDL-C levels resulted in greater thoracic aortic plaque regression compared to standard therapy, which was correlated with hsCRP reduction, suggesting that intensive statin therapy could provide better clinical outcomes., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

To elucidate the associations between Lp(a) levels and coronary and aortic atherosclerosis, we performed aortic MRI in 143 patients undergoing coronary angiography. Severity of aortic atherosclerosis was represented as plaque scores. Of the 143 patients, 104 had coronary artery disease (CAD). Thoracic and abdominal aortic plaques were found in 89 and 131 patients. Lp(a) levels increased stepwise with the number of stenotic coronary vessels: 15.7 (CAD(-)), 21.2 (1-vessel), 21.4 (2-vessel), and 22.9 mg/dl (3-vessel) (P<0.05). For aortic atherosclerosis, 143 patients were divided into quartiles by plaque scores. Lp(a) did not differ among quartiles of thoracic plaques: 17.1, 19.0, 23.5, and 21.2 mg/dl (P=NS), whereas Lp(a) increased stepwise with quartiles of abdominal plaques: 17.1, 19.2, 19.1, and 24.0 mg/dl (P<0.05). Lp(a) was an independent factor for CAD and abdominal aortic plaques, but not thoracic plaques. Thus, Lp(a) levels were associated with aortic atherosclerosis, especially in abdominal aorta, as well as coronary atherosclerosis., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Matrix metalloproteinases (MMPs) play a role in collagen breakdown, leading to plaque instability. High levels of MMPs mRNA and proteins, especially MMP-1, MMP-2, MMP-8, MMP-9, and MMP-13, were shown in human atherosclerotic plaques. However, among various MMPs, only MMP-1, MMP-8 and MMP-13, so-called interstitial collagenases, can initiate collagen breakdown. To elucidate whether MMP-1, MMP-8 and MMP-13 levels in blood were high in patients with unstable angina (UAP), we measured serum MMP-1 and plasma MMP-8 and MMP-13 levels in 45 patients with UAP, 175 with stable coronary artery disease (CAD), and 45 controls. Plasma C-reactive protein levels tended to be higher in patients with UAP than in those with stable CAD and controls (median 0.94 vs. 0.69 and 0.51mg/l). Regarding blood levels of MMPs, MMP-13 levels were above the lower detection limit in only one patient with UAP (2%), one with stable CAD (1%), and none in controls. MMP-1 levels did not differ among patients with UAP, stable CAD, and controls (median 4.8, 5.3, and 5.4ng/ml). Notably, MMP-8 levels were higher in patients with stable CAD than in controls (median 3.5ng/ml vs. 2.8ng/ml, P<0.005), however, MMP-8 levels in patients with UAP were much higher than those in stable CAD (3.9ng/ml vs. 3.5ng/ml, P<0.05). In multivariate analysis, MMP-8 level was an independent factor for UAP. Thus, plasma MMP-8 levels were found to be high in patients with UAP, suggesting that MMP-8 levels in UAP may reflect coronary plaque instability and that MMP-8 is a promising biomarker for UAP.

High-sensitivity C-reactive protein (hsCRP) levels can predict cardiovascular events among apparently healthy individuals and patients with coronary artery disease (CAD). However, hsCRP levels vary among ethnic populations. We previously reported hsCRP levels in Japanese to be much lower than in Western populations. We investigated the prognostic value of hsCRP levels in Japanese patients with stable CAD. The hsCRP levels were measured in 373 Japanese patients who underwent elective coronary angiography and thereafter decided to receive only medical treatment. Patients were followed up for 2.9+/-1.5 years for major cardiovascular events (death, myocardial infarction, unstable angina, stroke, aortic disease, peripheral arterial disease, or heart failure). The median hsCRP level was 0.70 mg/l. During the follow-up, cardiovascular events occurred in 53 (14%) of the 373 patients. Compared with 320 patients without events, 53 with events had higher hsCRP levels (median 1.06 vs. 0.67 mg/l, P<0.05). To clarify the association between hsCRP levels and cardiovascular events, the 373 study patients were divided into tertiles according to hsCRP levels: lower (<0.4 mg/l), middle (0.4-1.2mg/l), and higher (>1.2mg/l). The Kaplan-Meier analysis demonstrated a significant difference in the event-free survival rate between higher vs. middle or lower tertiles (P<0.05). In multivariate Cox regression analysis, the hsCRP level of >1.0mg/l was an independent predictor for cardiovascular events (hazard ratio, 2.0; 95%CI, 1.1-3.4; P<0.05). Thus, in Japanese patients with stable CAD who received only medical treatment, higher hsCRP levels, even >1.0mg/l, were found to be associated with a significantly increased risk for further cardiovascular events.

Fibrates reduce triglycerides (TG) and increase HDL-cholesterol levels, but there was no report showing plaque regression by fibrates. Using MRI, we investigated the effects of bezafibrate on aortic plaques in 22 dyslipidemic patients. All patients were asked to receive 400mg bezafibrate, but 8 who declined to have bezafibrate became the control group. Changes in vessel wall area (VWA) and lumen area (LA) from baseline to 1-year were evaluated. Bezafibrate reduced TG (-55%) and increased HDL-cholesterol levels (+29%). Bezafibrate reduced HDL size and increased LDL size. In thoracic plaques, bezafibrate reduced VWA (-6%, P<0.001) with no LA change, but VWA slightly progressed without bezafibrate (+5%). In abdominal plaques, bezafibrate reduced VWA (-8%, P<0.001) with LA increase (+3%, P<0.02), but VWA progressed without bezafibrate (+6%). VWA changes in thoracic and abdominal plaques correlated with TG reduction and HDL-cholesterol increase. Notably, VWA change in only abdominal plaques correlated with HDL size reduction and LDL size increase. Thus, bezafibrate induced plaque regression in thoracic and abdominal aortas with marked TG reduction and HDL-cholesterol increase, but the processes of plaque regression and vascular remodeling may differ between thoracic and abdominal aortas. However, because our study was not a controlled, randomized trial, further study is needed.

High-sensitivity C-reactive protein (hs-CRP) levels vary remarkably by race and ethnic group. We examined hs-CRP levels and their association with cardiovascular risk factors in the Japanese general population. The Japan National Cardiovascular Center (NCVC)-collaborative Inflammation Cohort (JNIC) Study recruited 5213 men and 7071 women aged > or = 40 years from seven communities in Japan during 2002-2004. hs-CRP was measured using nephelometry calibrated with CRM 470, the international plasma protein reference material. Traditional cardiovascular risk factors and their aggregation were studied in multivariate logistic models, stratified by overweight status. Median hs-CRP levels in men and women were 0.60 and 0.45 mg/L, respectively. The percentage of subjects with hs-CRP levels < 1.0, 1.0-3.0, and > 3.0 mg/L was 67.4%, 22.0%, and 10.6% in men, respectively, and 76.3%, 16.7%, and 7.0% in women. hs-CRP levels showed significant linear associations with traditional risk factors. Overweight, hypertension, dyslipidemia (men only), smoking (men only), and diabetes (women only) contributed significantly to elevated hs-CRP levels. Overweight individuals with hypertension, dyslipidemia, and diabetes had a high prevalence of elevated hs-CRP levels in both sexes. Japanese adults have very low hs-CRP levels. An aggregation of metabolic risk factors is associated with elevated hs-CRP levels among overweight individuals, particularly in women.

The association between coronary artery disease (CAD) and thoracic aortic plaques has often been reported using transesophageal echocardiography. However, studies showing the association between CAD and abdominal aortic plaques are scarce. CMR can visualize plaques in both the thoracic and abdominal aortas. Using CMR, we investigated the associations of thoracic and abdominal aortic plaques with the presence and extent of coronary artery stenosis in 146 patients undergoing coronary angiography, of whom 108 had CAD. The prevalence of thoracic and abdominal aortic plaques was higher in patients with CAD than in those without CAD (73% and 94% vs. 32% and 79%, p < 0.025). Stepwise increases in the prevalence and extents of both thoracic and abdominal plaques were found depending on the number of stenotic coronary vessels. Plaque extent in the thoracic aorta correlated with the numbers of > 50% and > 25% stenotic coronary segments (rs = 0.30 and 0.41). Plaque extent in the abdominal aorta also correlated with the numbers of > 50% and > 25% stenotic segments (rs = 0.40 and 0.44). Notably, the total plaque extent in the aortas correlated best with the numbers of > 50% and > 25% stenotic coronary segments (rs = 0.41 and 0.49, p < 0.001), and this factor was found to be the best predictor for the presence of CAD by the receiver-operating-characteristics curve analysis. Thus, the total plaque extent in the aortas was found to be more closely associated with the presence and extent of coronary stenosis than the thoracic or abdominal aortic plaque extent.

Prospective studies showed plasma high sensitivity C-reactive protein (hsCRP) levels to be a powerful predictor of cardiac events. However, the association between hsCRP levels and the extent of coronary stenosis in patients with coronary artery disease (CAD) remains controversial. We investigated the association between hsCRP levels and the extent of coronary stenosis in 273 patients undergoing elective coronary angiography. Plasma hsCRP levels were higher in patients with CAD than in those without CAD (0.70 mg/l versus 0.56 mg/l, P < 0.02), but hsCRP levels did not correlate with the number of >50% stenotic vessels and were not a significant factor for CAD. However, after the exclusion of 76 patients taking statins, a step-wise increase in hsCRP levels was found depending on the number of >50% stenotic vessels: 0.50 in CAD(-), 0.68 in 1-vessel, 0.77 in 2-vessel, and 0.88 mg/l in 3-vessel disease (P < 0.01). The hsCRP levels also correlated with the numbers of >50% and >25% stenotic segments (r = 0.30 and 0.32, P < 0.001). Multivariate analysis revealed the hsCRP levels to be a significant factor for CAD. Thus, after the exclusion of patients with statins, plasma hsCRP levels were found to be associated with the presence and extent of coronary stenosis in patients with stable CAD.

Mycoplasma pneumoniae (MP) seropositivity was reported to be associated with coronary events. MP organisms were detected with Chlamydia pneumoniae (CP) in coronary plaques. We investigated MP and CP seropositivity in 549 patients undergoing coronary angiography. Coronary artery disease (CAD) was found in 396 patients, of whom 154 had myocardial infarction (MI). MP seropositivity was more prevalent in patients with CAD than without CAD (14% versus 6%, P < 0.01). The highest prevalence was found in patients with MI. In contrast, the prevalence of CP seropositivity was similar in patients with and without CAD (62% versus 59%). To clarify interaction with CP infection, 549 patients were divided into two groups with and without CP seropositivity. Among patients with CP seropositivity, MP seropositivity was more prevalent in patients with CAD than without CAD (17% versus 5%, P < 0.01), whereas among patients without CP seropositivity, MP seropositivity did not differ between patients with and without CAD (9% versus 6%). In multivariate analysis, MP seropositivity was associated with CAD only in patients with CP seropositivity (odds ratio = 5.1, 95% CI = 1.8-14.9). Thus, MP seropositivity was associated with CAD. However, this association was confined to patients with CP seropositivity. Coinfection by MP and CP may be an important cofactor for CAD.

Diabetes was reported to be associated with a mitochondrial (mt) DNA mutation at 3243 and variants at 1310, 1438, 3290, 3316, 3394, 12,026, 15,927, and 16,189. Among these mtDNA abnormalities, those at 3243, 3316, 15,927, and 16,189 were also suggested to cause cardiomyopathies. We investigated the prevalence of such mtDNA abnormalities in 68 diabetic patients with LV hypertrophy (LVH), 100 without LVH, and 100 controls. Among the 9 mtDNA abnormalities, those at 3243, 3316, and 15,927 tended to be more prevalent in diabetic patients with LVH than in those without LVH (1%, 1%, and 4% vs. 0%, 0%, and 0%). Notably, the variant at 16,189 was more prevalent in diabetic patients with LVH than without LVH (46% vs. 24%, [Formula: see text] ). The odds ratio for LVH was 3.0 (95% CI, 1.5-6.1) for the 16,189 variant. A common mtDNA variant at 16,189 was found to be associated with LVH in diabetic patients.

Recently, osteopontin (OPN) mRNA was reported to be highly expressed in atherosclerotic plaques, most strikingly in calcified plaques. We examined if plasma OPN levels are associated with coronary stenosis and calcification in patients with coronary artery disease (CAD). We measured plasma OPN levels in 178 patients undergoing coronary angiography. Compared with 71 patients without CAD, 107 with CAD had higher OPN levels (616+/-308 ng/ml versus 443+/-237 ng/ml, P<0.001). A stepwise increase in OPN levels was found depending on the number of >50% stenotic coronary vessels: 540+/-293 ng/ml in 1-vessel, 615+/-230 ng/ml in 2-vessel, and 758+/-416 ng/ml in 3-vessel disease. OPN levels also correlated with the numbers of >50% and >25% stenotic segments (r=0.35 and 0.43, respectively, P<0.001). In multivariate analysis, OPN levels were significantly associated with CAD (odds ratio=1.21, 95% CI=1.05-1.39 for a 100 ng/ml increase) independent of traditional risk factors. Coronary calcification was found in 86 patients. OPN levels were higher in patients with calcification than in those without calcification (608+/-328 ng/ml versus 490+/-246 ng/ml, P<0.01) and correlated with the number of calcified segment (r=0.26, P<0.001). However, OPN levels were not independently associated with coronary calcification. Thus, plasma OPN levels were found to be associated with the presence and extent of CAD.

A 63-year-old woman with abnormal Q waves in leads II, III, aVF developed ventricular tachycardia after an operation for thyroid carcinoma. Coronary arteriography revealed no organic stenosis, but acetylcholine induced total occlusion of the right coronary artery and severe narrowing of the left coronary artery. Left ventriculography showed inferoposterior and septal akinesis, and echocardiography revealed slight thinning of these affected walls. She had old myocardial infarction due to spasm. One year later, she developed bilateral uveitis and recurrence of tachycardia. Cardiac sarcoidosis was diagnosed by endomyocardial biopsy. In our patient with cardiac sarcoidosis, the presence of multivessel coronary spasm made the diagnosis difficult and may have contributed to cardiac dysfunction. Coronary arteries are rarely involved, but the development of coronary spasm may be linked to sarcoidosis.

Widening of the aortic shadow on chest radiography is one of the first indicators of aortic dissection. The degree of widening of the aortic shadow was estimated on two successive chest radiographs (mean [+/-SD] interval 0.8 +/- 0.7 years) before and after aortic dissection in 11 patients (four with DeBakey classification type I, seven with type III dissection). The distance between the center of each thoracic vertebra and the lateral margin of the descending aortic shadow (L) was measured. Since only a supine frontal film is usually available in acute aortic dissection, chest radiographs in both erect and supine positions were compared in 18 patients with hypertension. On supine films, L was larger than that on erect films, but the difference (delta L) was minimal (+2.6 mm) at the level of the tracheal bifurcation. Therefore, the L at the level of tracheal bifurcation (Lb) was best suited for comparing films taken in different positions. On supine films, Lb was significantly longer in patients with aortic dissection than in patients with hypertension (60.5 +/- 8.2 vs 46.0 +/- 7.9 mm, p < 0.001), and none with dissection showed Lb < 50 mm. Serial change of L over the follow-up of 1.4 +/- 0.7 years in patients with hypertension was also examined in erect films and was less than +1 mm. When the index film in a supine position was compared with the previous films in an erect position, delta Lb in patients with aortic dissection was +12.7 +/- 5.6 mm, which was significantly greater than that in patients with hypertension (+2.9 +/- 2.8 mm, p < 0.001). All 11 patients with aortic dissection showed delta Lb > or = +7 mm, but only one patient with hypertension (6%) exhibited this finding. Chest radiography is useful for identifying patients with aortic dissection, who characteristically show Lb > or = 50 mm on presentation and delta Lb > or = +7 mm, compared with previous films.

The instant of cardiac rupture was initially recorded using two-dimensional echocardiography in a patient with acute myocardial infarction. This 70-year-old woman was admitted to our hospital because of chest pain lasting for six hours. The admission electrocardiogram showed Q waves and S-T segment elevations in leads I, aVL, and V4-6. Two-dimensional echocardiography revealed hypokinesis in the middle and apical portions of the anterior septum and hyperkinesis in the basal portion of the anterior septum and the posterior wall. When the patient suddenly lost consciousness, echocardiography detected a rapidly developing pericardial effusion, which filled the pericardial sac within 13 sec. A myocardial tear was recognized at the apex of the left ventricle between portions of the hypokinesis and hyperkinesis. A simultaneously-recorded electrocardiogram showed sinus rhythm (84/min) which did not change at the moment of rupture and lasted further for 15 sec until a sudden alteration to sinus bradycardia (46/min) occurred. Cardio-pulmonary resuscitation was unsuccessful and the patient died. This is the first such case in the medical literature in which the instant of cardiac rupture was recorded. Detailed reviews of the video tapes revealed that rapid accumulation of pericardial fluid occurred, followed by transient sinus bradycardia, most likely due to vagal reflex to the stretched pericardium.