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Background: Cardiac rupture is a major lethal complication of acute myocardial infarction (MI). Despite significant advances in reperfusion strategies, mortality from cardiac rupture remains high. Studies suggest that cardiac rupture can be accelerated by thrombolytic therapy, but the relevance of this risk factor remains controversial., Methods: We analyzed protease-activated receptor 4 (Par4) expression in mouse hearts with MI and investigated the effects of Par4 deletion on cardiac remodeling and function after MI by echocardiography, quantitative immunohistochemistry, and flow cytometry., Results: Par4 mRNA and protein levels were increased in mouse hearts after MI and in isolated cardiomyocytes in response to hypertrophic and inflammatory stimuli. Par4-deficient mice showed less myocyte apoptosis, reduced infarct size, and improved functional recovery after acute MI relative to wild-type (WT). Conversely, Par4 -/- mice showed impaired cardiac function, greater rates of myocardial rupture, and increased mortality after chronic MI relative to WT. Pathological evaluation of hearts from Par4 -/- mice demonstrated a greater infarct expansion, increased cardiac hemorrhage, and delayed neutrophil accumulation, which resulted in impaired post-MI healing compared with WT. Par4 deficiency also attenuated neutrophil apoptosis in vitro and after MI in vivo and impaired inflammation resolution in infarcted myocardium. Transfer of Par4 -/- neutrophils, but not of Par4 -/- platelets, in WT recipient mice delayed inflammation resolution, increased cardiac hemorrhage, and enhanced cardiac dysfunction. In parallel, adoptive transfer of WT neutrophils into Par4 -/- mice restored inflammation resolution, reduced cardiac rupture incidence, and improved cardiac function after MI., Conclusions: These findings reveal essential roles of Par4 in neutrophil apoptosis and inflammation resolution during myocardial healing and point to Par4 inhibition as a potential therapy that should be limited to the acute phases of ischemic insult and avoided for long-term treatment after MI.

Rationale: Cardiac angiosarcoma is the most common malignant tumor of the heart and a rare disease with rapid disease progression and poor prognosis. Cardiac wall rupture is an extremely rare complication., Patient Concerns: A 32-year-old woman presented with an acute onset of epigastric pain and chest discomfort at first time when she visited an emergency room., Diagnoses: A cardiac mass was identified on echocardiography and subsequently performed chest computed tomography and cardiac magnetic resonance imaging revealed the cardiac tumor at right atrium with right atrial wall rupture and hematogenous lung metastasis. Histopathologic diagnosis of metastatic angiosarcoma was done by open lung biopsy., Interventions: The patient was treated with palliative chemotherapy for the primary cardiac tumor and hematogenous lung metastasis., Outcomes: The follow-up imaging studies revealed treatment response of the primary cardiac tumor and hematogenous lung metastasis., Lessons: Clinical and radiologic evaluation of the cardiac angiosarcoma was well performed in our case with various diagnostic imaging modalities including echocardiography, chest computed tomography, cardiac magnetic resonance imaging, and fluorodeoxyglucose-positron emission tomography/computed tomography. This case report well demonstrates typical imaging findings of a rare cardiac tumor and emphasizes importance of early investigation for accurate diagnosis and proper management of the cardiac tumor.

Rationale: Ruptured aneurysm originating from the left coronary sinus of Valsalva into the left ventricle (LV) is extremely rare. Imaging features of sinus aneurysm has been commonly reported using echocardiography or angiography. Here, we report multidetector computed tomography (MDCT) findings of left sinus of Valsalva aneurysm extending into the LV and caused severe aortic regurgitation (AR) in a 44-year-old male with latent infective endocarditis. The role of MDCT in preoperative surgical planning was also emphasized., Patient Concerns: The patient visited our hospital due to worsening exertional dyspnea for 3 months., Diagnoses: On cardiac computed tomography (CT) using 320-MDCT, a saccular aneurysm arising from the left coronary sinus of Valsalva extending into the LV was diagnosed as the cause of severe AR., Interventions: The patient underwent resection of the aneurysm, aortic root reconstruction, and aortic valve replacement., Outcomes: The patient made an uneventful recovery. Follow-up echocardiography showed no paravalvular leakage with improved LV function., Lessons: MDCT with wide coverage and high temporal resolution can provide exact and comprehensive information about complicated conditions, leading to confident surgical planning and successful management.

Ventricular free wall rupture (VFWR) is the second most common cause of death in patients with acute ST-elevation myocardial infarction (STEMI). Nevertheless, few reports have investigated the factors, including different treatment strategies, associated with VFWR in Taiwanese patients. Therefore, the aim of this study was to compare the risk of VFWR in Taiwanese patients with acute STEMI who had received primary percutaneous coronary intervention (PCI), rescue PCI, scheduled PCI, thrombolytic therapy, and pharmacologic treatment. In this medical records review study, records of patients with acute STEMI admitted to a regional hospital in south Taiwan between March 1999 and October 2013 were screened. Multivariate stepwise logistic regression analysis was used to evaluate the association between the risk of VFWR and its independent factors. The overall incidence of VFWR among the 1545 patients with acute STEMI in this study was 1.6%. Compared with primary PCI, the risk of VFWR was significantly higher in patients who had received thrombolysis (adjusted odds ratio = 6.83, P = 0.003) or pharmacologic treatment alone (adjusted odds ratio = 3.68, P = 0.014). The risk of VFWR in patients receiving rescue PCI or scheduled PCI was not significantly different from that in patients receiving primary PCI. In addition, older age and Killip class >I were associated with an increased risk of VFWR in patients with acute STEMI, whereas the use of angiotensin-converting enzyme inhibitors was associated with a lower risk of VFWR. In conclusion, findings from this medical record review study provide support for the use of primary PCI, rescue PCI, and scheduled PCI over thrombolytic therapy and pharmacologic treatment in reducing the risk of VFWR in Taiwanese patients with acute STEMI.

Background: Immune cell-mediated inflammation is an essential process for mounting a repair response after myocardial infarction (MI). The sympathetic nervous system is known to regulate immune system function through β-adrenergic receptors (βARs); however, their role in regulating immune cell responses to acute cardiac injury is unknown., Methods: Wild-type (WT) mice were irradiated followed by isoform-specific βAR knockout (βARKO) or WT bone-marrow transplantation (BMT) and after full reconstitution underwent MI surgery. Survival was monitored over time, and alterations in immune cell infiltration after MI were examined through immunohistochemistry. Alterations in splenic function were identified through the investigation of altered adhesion receptor expression., Results: β2ARKO BMT mice displayed 100% mortality resulting from cardiac rupture within 12 days after MI compared with ≈20% mortality in WT BMT mice. β2ARKO BMT mice displayed severely reduced post-MI cardiac infiltration of leukocytes with reciprocally enhanced splenic retention of the same immune cell populations. Splenic retention of the leukocytes was associated with an increase in vascular cell adhesion molecule-1 expression, which itself was regulated via β-arrestin-dependent β2AR signaling. Furthermore, vascular cell adhesion molecule-1 expression in both mouse and human macrophages was sensitive to β2AR activity, and spleens from human tissue donors treated with β-blocker showed enhanced vascular cell adhesion molecule-1 expression. The impairments in splenic retention and cardiac infiltration of leukocytes after MI were restored to WT levels via lentiviral-mediated re-expression of β2AR in β2ARKO bone marrow before transplantation, which also resulted in post-MI survival rates comparable to those in WT BMT mice., Conclusions: Immune cell-expressed β2AR plays an essential role in regulating the early inflammatory repair response to acute myocardial injury by facilitating cardiac leukocyte infiltration., (© 2016 American Heart Association, Inc.)

Rationale: Matrix metalloproteinase (MMP)-28 regulates the inflammatory and extracellular matrix responses in cardiac aging, but the roles of MMP-28 after myocardial infarction (MI) have not been explored., Objective: To determine the impact of MMP-28 deletion on post-MI remodeling of the left ventricle (LV)., Methods and Results: Adult C57BL/6J wild-type (n=76) and MMP null (MMP-28((-/-)), n=86) mice of both sexes were subjected to permanent coronary artery ligation to create MI. MMP-28 expression decreased post-MI, and its cell source shifted from myocytes to macrophages. MMP-28 deletion increased day 7 mortality because of increased cardiac rupture post-MI. MMP-28(-/-) mice exhibited larger LV volumes, worse LV dysfunction, a worse LV remodeling index, and increased lung edema. Plasma MMP-9 levels were unchanged in the MMP-28((-/-)) mice but increased in wild-type mice at day 7 post-MI. The mRNA levels of inflammatory and extracellular matrix proteins were attenuated in the infarct regions of MMP-28(-/-) mice, indicating reduced inflammatory and extracellular matrix responses. M2 macrophage activation was impaired when MMP-28 was absent. MMP-28 deletion also led to decreased collagen deposition and fewer myofibroblasts. Collagen cross-linking was impaired as a result of decreased expression and activation of lysyl oxidase in the infarcts of MMP-28(-/-) mice. The LV tensile strength at day 3 post-MI, however, was similar between the 2 genotypes., Conclusions: MMP-28 deletion aggravated MI-induced LV dysfunction and rupture as a result of defective inflammatory response and scar formation by suppressing M2 macrophage activation.

Cardiac herniation as a result of traumatic pericardial rupture is a serious injury and a difficult diagnosis to make on radiographic studies. Even with the more advanced imaging modalities, this rare diagnosis remains challenging. In a high-energy traumatic setting, there are chest radiograph and multidetector computed tomography findings that are strongly suggestive of cardiac herniation. The imaging, along with greater awareness of this injury, may provide a more rapid diagnosis, thus potentially preventing the severe clinical deterioration often seen in these patients.

The cardiac extracellular matrix is a dynamic structural support network that is both influenced by, and a regulator of, pathological remodeling and hypertrophic growth. In response to pathologic insults, the adult heart reexpresses the secreted extracellular matrix protein periostin (Pn). Here we show that Pn is critically involved in regulating the cardiac hypertrophic response, interstitial fibrosis, and ventricular remodeling following long-term pressure overload stimulation and myocardial infarction. Mice lacking the gene encoding Pn (Postn) were more prone to ventricular rupture in the first 10 days after a myocardial infarction, but surviving mice showed less fibrosis and better ventricular performance. Pn(-/-) mice also showed less fibrosis and hypertrophy following long-term pressure overload, suggesting an intimate relationship between Pn and the regulation of cardiac remodeling. In contrast, inducible overexpression of Pn in the heart protected mice from rupture following myocardial infarction and induced spontaneous hypertrophy with aging. With respect to a mechanism underlying these alterations, Pn(-/-) hearts showed an altered molecular program in fibroblast function. Indeed, fibroblasts isolated from Pn(-/-) hearts were less effective in adherence to cardiac myocytes and were characterized by a dramatic alteration in global gene expression (7% of all genes). These are the first genetic data detailing the function of Pn in the adult heart as a regulator of cardiac remodeling and hypertrophy.

Background: Class A macrophage scavenger receptor (SR-A) is a macrophage-restricted multifunctional molecule that optimizes the inflammatory response by modulation of the activity of inflammatory cytokines. This study was conducted with SR-A-deficient (SR-A(-/-)) mice to evaluate the relationship between SR-A and cardiac remodeling after myocardial infarction., Methods and Results: Experimental myocardial infarction (MI) was produced by ligation of the left coronary artery in SR-A(-/-) and wild-type (WT) male mice. The number of mice that died within 4 weeks after MI was significantly greater in SR-A(-/-) mice than in WT mice (P=0.03). Importantly, death caused by cardiac rupture within 1 week after MI was 31% (17 of 54 mice) in SR-A(-/-) mice and 12% (6 of 51 mice) in WT mice (P=0.01). In situ zymography demonstrated augmented gelatinolytic activity in the infarcted myocardium in SR-A(-/-) mice compared with WT mice. Real-time reverse transcription-polymerase chain reaction at day 3 after MI showed that the expression of matrix metalloproteinase-9 mRNA increased significantly in the infarcted myocardium in SR-A(-/-) mice compared with WT mice. Furthermore, SR-A(-/-) mice showed augmented expression of tumor necrosis factor-alpha and reduction of interleukin-10 in the infarcted myocardium at day 3 after MI. In vitro experiments also demonstrated increased tumor necrosis factor-alpha and decreased interleukin-10 expression in activated SR-A(-/-) macrophages., Conclusions: The present findings suggest that SR-A deficiency might cause impairment of infarct remodeling that results in cardiac rupture via insufficient production of interleukin-10 and enhanced expression of tumor necrosis factor-alpha and of matrix metalloproteinase-9. SR-A might contribute to the prevention of cardiac rupture after MI.

The takotsubo syndrome is a clinical entity that can mimic an acute myocardial infarction. It is characterised by anginal chest pain with ST-T elevation in precordial leads, without coronary obstruction at angiography; its distinctive feature is a peculiar pattern of left ventricular contraction, with expansion of the apical segments and basal hyperkinesis, also known as 'apical ballooning'. This syndrome usually has a good prognosis, with normalisation of the left ventricular contraction impairment within several days, although Japanese authors have described two cases of free left ventricular wall rupture in these patients.We describe a case of apical ballooning syndrome complicated by left ventricular rupture in a Caucasian old female. To our knowledge, this is the first-ever case of a fatal outcome in the Caucasian population, due to free wall ventricular rupture, and confirms that the takotsubo syndrome may lead to a fatal cardiac event.

A 15-year-old male died of cardiac rupture due to blunt chest trauma from a traffic accident involving a low-speed scooter carrying 3 people and a head-on collision with a tree. The victim was sitting on the footrest of the scooter. It was concluded that the victim was compressed between the handlebar of the scooter and the other 2 passengers, causing cardiac ruptures via bidirectional compression and intravascular hydrostatic pressure. The victim may have served as a cushion for the other 2 passengers, who were not thrown from the scooter and sustained only minor injuries.

Background: We investigated the potential contributions of tumor necrosis factor-alpha (TNF-alpha) on the incidence of acute myocardial rupture and subsequent chronic cardiac dysfunction after myocardial infarction (MI) in TNF knockout (TNF-/-) mice compared with C57/BL wild-type (WT) mice., Methods and Results: Animals were randomized to left anterior descending ligation or sham operation and killed on days 3, 7, 14, and 28. We monitored cardiac rupture rate, cardiac function, inflammatory response, collagen degradation, and net collagen formation. We found the following: (1) within 1 week after MI, 53.3% (n=120) of WT mice died of cardiac rupture, in contrast to 2.5% (n=80) of TNF-/- mice; (2) inflammatory cell infiltration and cytokine expression were significantly higher in the infarct zone in WT than TNF-/- mice on day 3; (3) matrix metalloproteinase-9 and -2 activity in the infarcted myocardium was significantly higher in WT than in TNF-/- mice on day 3; (4) on day 28 after MI compared with sham, there was a significant decrease in LV developed pressure (74%) and +/-dP/dt(max) (68.3%/65.3%) in WT mice but a less significant decrease in +/-dP/dt(max) (25.8%/28.8%) in TNF-/- mice; (5) cardiac collagen volume fraction was lower in WT than in TNF-/- mice on days 3 and 7 but higher on day 28 compared with TNF-/- mice; and (6) a reduction in myocyte apoptosis in TNF-/- mice occurred on day 28 compared with WT mice., Conclusions: Elevated local TNF-alpha in the infarcted myocardium contributes to acute myocardial rupture and chronic left ventricle dysfunction by inducing exuberant local inflammatory response, matrix and collagen degradation, increased matrix metalloproteinase activity, and apoptosis.

Background: Recently, it was reported that the degree of microvascular injury and left ventricular functional recovery during the chronic period can be predicted after treatment of the infarct-related artery based on the coronary flow velocity (CFV) pattern assessed using a Doppler guidewire. The aim of this prospective study was to examine whether the CFV pattern may predict complications and in-hospital survival after acute myocardial infarction (AMI)., Methods and Results: The study population consisted of 169 consecutive patients with a first anterior AMI successfully treated with percutaneous coronary intervention (PCI). We examined the CFV pattern immediately after PCI using a Doppler guidewire. In accordance with previous findings, we defined severe microvascular injury as a diastolic deceleration time < or =600 ms and the presence of systolic flow reversal. Patients were divided into two groups: those without severe microvascular injury (n=118; group 1) and those with severe microvascular injury (n=51; group 2). All of the patients who had cardiac rupture were in group 2. Congestive heart failure (CHF) was observed more frequently in group 2 than in group 1 (53% versus 8%, P<0.001). The in-hospital cardiac mortality rate was significantly higher in group 2 than in group 1 (18% versus 0%, P<0.001). Nine patients in group 2 died, 5 patients because of CHF and 4 patients because of cardiac rupture., Conclusions: These findings suggest that the CFV pattern is an accurate predictor of the presence or absence of complications and of in-hospital survival after AMI.

Setting: The collapse of a patient immediately after right pneumonectomy with right pericardiotomy resulted in closed-chest cardiopulmonary resuscitation, subsequent thoracotomy, and demise secondary to right ventricular rupture., Interventions: Closed-chest resuscitation with opened and closed chest tubes and medical and fluid interventions were inadequate, necessitating subsequent thoracotomy., Main Results and Conclusions: Right ventricular rupture during resuscitation was found during subsequent thoracotomy. This rupture and inadequacy of closed-chest resuscitation were felt to be associated with the operative pneumonectomy and pericardiotomy. Pathophysiology and the role of open-heart vs. closed-chest resuscitative measures are discussed.

Background: Pump failure after acute myocardial infarction (AMI) can be predicted by several indices that estimate infarct size. However, there are few indices that predict infarct expansion and cardiac rupture. We focused on the prognostic significance of serum C-reactive protein (CRP) after AMI., Methods and Results: Serum CRP levels were measured every 24 hours in 220 patients with a first Q-wave AMI. In-hospital complications, predischarge left ventriculographic findings, and long-term prognosis were assessed in relation to peak CRP levels. Peak levels of both CRP and creatine kinase (CK) were higher in patients with pump failure than in those without pump failure. In patients with cardiac rupture, peak CRP levels were higher than in those without rupture (P=.001); peak CK levels were not predictive. Higher CRP levels were found in patients with left ventricular aneurysm (P=.001 versus those without), aggravated heart failure (P=.03 versus those without), and cardiac death (P<.0001 versus survivors) during the first year after AMI. Multivariate analysis confirmed that an elevation of the peak CRP level > or = 20 mg/dL was an independent predictor of cardiac rupture (relative risk, 4.72; P=.004), left ventricular aneurysmal formation (relative risk, 2.11; P=.03), and 1-year cardiac death (relative risk, 3.44; P<.0001)., Conclusions: Cardiac rupture, left ventricular aneurysmal formation, and 1-year cardiac death were associated with an elevation of serum CRP early after AMI, suggesting that elevation of CRP levels after AMI may predict infarct expansion.

The case of a patient with delayed mitral regurgitation and right coronary artery traumatic injury in association with intramyocardial dissection without rupture or pseudoaneurysm is presented. These findings evolved secondary to blunt chest trauma and were confirmed by cardiac ultrasound scanning, magnetic resonance imaging, and cardiac catheterization. Successful surgical correction was facilitated with this combination of diagnostic testing.

Blunt cardiac injury is frequently noted among trauma patients. They may demonstrate few signs and symptoms or may be in profound shock. A unique case of left ventricular disruption in a young soldier who sustained blunt torso trauma is reported. A paucity of clinical findings led to a delay in diagnosis. He ultimately underwent successful repair 12 days after injury.

Blunt chest trauma resulting in combined aortic disruption and cardiac rupture, although a common autopsy finding, was found reported only once previously in a surviving patient. We report two cases repaired through a left posterolateral thoracotomy in which the cardiac injury was unsuspected and presented as an intraoperative finding of hemopericardium. With improved emergency resuscitation in the field and faster transport of these cases to tertiary care centers, this combination of lesions may be seen more frequently. Suggestions for their diagnosis and management are presented.

Medical treatment of postinfarction ventricular septal rupture carries a high mortality. Delayed surgery can be done with good results but many patients die awaiting operation. In 1978 we decided that all such patients presenting to us should undergo urgent cardiac catheterization and surgery. Since then we have seen 22 such patients. Two decided against surgery and died in the hospital. Twenty agreed to surgery; in 15 of these an intra-aortic balloon pump was inserted before catheterization and in another four at the time of operation. Catheterization was performed without complication, and surgery was performed within 2 days of septal rupture in all 20 patients. Twelve patients (60%) survived hospitalization. Three patients died of pump failure shortly after surgery; five died after a second operation for free wall rupture (n = 2) or persistent or recurrent septal defect (n = 3). Two other patients survived reoperation. Survivors were significantly younger than nonsurvivors and had a higher cardiac index and a lower shunt ratio. At a mean follow-up of 47.9 months, there has been one late noncardiac death. Eleven patients survive, all in class I or II. We conclude that in patients with septal rupture urgent surgery results in improved near-term survival compared with known survival rates in medically treated patients. Early recurrent rupture is common and often disastrous and requires refinement in operative technique. Age, cardiac index, and shunt volume are related to surgical outcome. Hospital survivors do very well on a long-term basis. We recommend continuation of this aggressive approach.

Right ventricular rupture is rare. We report its identification by radionuclide ventriculography and subsequent confirmation by contrast angiography and at operation. The aetiology in this case was a primary cardiac malignancy.

We compared two methods of delivering single damped sine-wave defibrillator pulses to the coronary sinus orifice in 20 dogs. Ten dogs had "unipolar" (coronary sinus to precordial disc) and 10 had "bipolar" (coronary sinus proximal to coronary sinus distal electrode) discharges. Delivered voltage, current, and energy were recorded during each pulse. Electrophysiologic testing was done before and 4 weeks after the procedure. Histologic examination of the atrioventricular groove was done at 1 mm serial sections. For the unipolar configuration a 200 J defibrillator pulse resulted in a peak voltage of 3370 +/- 125 V, a peak current of 21 +/- 4 A, and a delivered energy of 253 +/- 29 J as compared with 3010 +/- 99 V, 70 +/- 4 A, and 144 +/- 18 J, respectively, for the bipolar configuration (p less than .001). Three dogs (two with bipolar, one with unipolar pulses) had gross coronary sinus rupture and died from acute pericardial tamponade. In addition, irrespective of electrode configuration, all dogs showed microscopic rupture of the coronary sinus internal elastic membrane. Transmural atrial scarring occurred in all 10 dogs that received a unipolar pulse but in only two dogs that received a bipolar pulse (p = .0004). Unlike the atrium, injury to the left ventricle was limited in both groups. Similarly, injury to the periannular myocardium was inconsistent and not transmural in either group. No significant electrophysiologic changes were observed. With the present technique, unipolar rather than bipolar catheter-mediated defibrillator pulses result in transmural atrial injury that might prevent accessory pathway conduction. Regardless of electrode configuration, high-energy defibrillator pulses consistently cause some degree of coronary sinus rupture, most likely related to a barotraumatic mechanism.

Fifty-five patients had surgical repair of postinfarction ventricular septal rupture in Massachusetts General Hospital from 1968 through 1981. In patients operated more than three weeks after infarction, hospital survival has been 93% (14/15). Before 1975 in patients operated less than three weeks after infarction, hospital survival was 41% (7/17). In this same era patents operated for septal rupture with cardiogenic shock present before operation had a hospital survival rate of only 27% (3/11). Before 1975 patients with cardiogenic shock were supported with intra-aortic balloon pumping (IABP) and vasopressors, and operation deferred pending hemodynamic stabilization. Before 1975 patients with anterior septal rupture had a hospital survival rate of 64% (9/14), while patients with posterior septal rupture had a hospital survival rate of only 38% (5/13). This difference in survival according to the location of septal rupture occurred despite comparable numbers of patients in each group requiring early operation, as well as incidence of cardiogenic shock. Since January 1, 1975 patients operated less than three weeks after infarction have had an overall hospital survival rate of 70% (16/23). Of the 10 most recent patients operated early, nine are survivors. In patients with anterior defects 85% (11/13) survived, while in patients with posterior defects 67% survived (10/15). In patients operated with cardiogenic shock present before operation, survival has been 67% (10/15). Changes in management leading to improved results include (1) immediate operation for patients with cardiogenic shock, (2) cold cardioplegic protection of the myocardium, and (3) prosthetic replacement of posterior left ventricular free wall defect, after infarctectomy and septal repair, in patients with posterior septal rupture.

Seven patients with cardiac rupture from blunt trauma were encountered at the University Hospital, University of Alabama School of Medicine, in a 15-year period. Five of seven patients survived, including three with left atrial injuries and one each with right ventricular and left ventricular injuries. Useful diagnostic features included systolic hypotension, distended neck veins, and elevated central venous pressures. Associated injuries averaged four per patient. Successful management demands a high index of suspicion of cardiac injury, prompt diagnosis, and immediate median sternotomy. After repair of the heart the incision should usually be extended to allow exploratory laparotomy.

Blunt injury to the heart ranges from contusion to disruption. This report comprises 14 patients seen during a 6-year period with cardiac rupture secondary to blunt trauma. Eight patients were injured in automobile accidents, two patients were injured in auto-pedestrian accidents, two were kicked in the chest by ungulates, and two sustained falls. Cardiac tamponade was suspected in ten patients. Five patients presented with prehospital cardiac arrest or arrested shortly after arrival. All underwent emergency department thoracotomy without survival. Two patients expired in the operating room during attempted cardiac repair; both had significant extracardiac injury. Seven patients survived, three had right atrial injuries, three had right ventricular injuries, and one had a left atrial injury. Cardiopulmonary bypass was not required for repair of the surviving patients. There were no significant complications from the cardiac repair. The history of significant force dispersed over a relatively small area of the precordium as in a kicking injury from an animal or steering wheel impact should alert the physician to possible cardiac rupture. Cardiac rupture should be considered in patients who present with signs of cardiac tamponade or persistent thoracic bleeding after blunt trauma.

False aneurysms of the left ventricle were repaired in four patients (average age, 61 years). The etiology was myocardial infarction in three patients and disruption of an apical left ventricular cannulation site in the fourth. The interval from initiating event to surgery averaged 11 months. One patient was in cardiogenic shock and succumbed in the operating room from myocardial failure. The other three patients, in functional class III at the time of surgery, survived and are currently asymptomatic. The literature records 43 patients who have undergone surgical repair of a false aneurysm of the left ventricle. The causes were myocardial infarction (12 patients), operative injury (13 patients), penetrating trauma (11 patients), and blunt trauma (seven patients). Twenty-seven (63%) were under the age of 50 years. In those who were limited by symptoms, congestive heart failure predominated. Forty seven per cent of the patients were operated upon in the first five months following the initiating event; 61% within the first year. Only four patients underwent surgery more than 48 months after the myocardial insult. Thrombus was present in 28% of the aneurysms. Morbidity was recorded in nine patients, and six patients (14%) died. This study documents the necessity for early surgical repair and the relatively low operative mortality obtained with this lethal lesion.

Five patients (four adults and one child) with clinically suspected myocardial perforation by temporary transvenous pacemakers were studied by real-time, two-dimensional echocardiography. In three patients, the catheters were visualized passing through the right ventricular apical wall with the tip located outside the cardiac border. In one patient the catheter perforated the atrioventricular septum and entered the left ventricle with the tip lodged against the posterior wall. In another patient, the catheter had partially penetrated the ventricular septum near the apex. Pericardial effusion was observed in two patients, in one of whom it was localized to the site of perforation. No patient had evidence of cardiac tamponade. In four patients, the catheters were withdrawn under echocardiographic visualization and the catheter tips could be seen moving from the abnormal locations back into the right-heart chambers. Perforation was verified at autopsy in two patients, including one in whom the catheter was not withdrawn. Real-time, two-dimensional echocardiography appears to be valuable in the diagnosis of pacemaker perforation.

Forty-one patients with postinfarction ventricular septal rupture were cared for in our hospital during 1971-1975. Cardiogenic shock developed after septal rupture in 55% of these patients. Shock was unrelated to site of infarction, extent of coronary artery disease, left ventricular ejection fraction, or pulmonary-to-systemic flow ratio, but mean pulmonary artery pressure was lower in shock than in nonshock patients. These observations suggest that shock was produced mainly by right ventricular impairment. Perioperative survival was much higher in patients who did not have shock preoperatively (14 of 17 [82+]) than in those who did (three of 11 [27%]). Magnitude of shunt, left ventricular ejection fraction, extent of coronary artery disease, and performance of aortocoronary bypass grafting were not distinctly correlated with perioperative survival. After a minimum 4-year follow-up, 76% of the perioperative survivors are alive, and none suffer more than New York Heart Association functional class II disability. All 13 unoperated patients (11 in shock) died within 3 months.

Forty-six patients who underwent mitral valve replacement for mitral regurgitation due to coronary artery disease during 1970-1975 were identified. Forty patients underwent aortocoronary bypass procedures at the same operation. The survival rate at the fourth postoperative year was 73% in the 22 patients in whom the preoperative left ventricular ejection fraction exceeded 0.35, 38% in the 16 patients in whom the preoperative left ventricular ejection fraction was 35% or less, and 25% in the eight patients in whom aneurysmectomy was performed at the time of mitral valve replacement (p less than 0.05 for the former group compared to the latter two groups). Heart failure, present preoperatively in 41 patients, was improved in most of the long-term survivors. Neither the angiographic extent of coronary artery disease nor whether mitral valve replacement was performed in the acute (within 2 months in 13 patients) or chronic phase of myocardial infarction were distinctly correlated with survival.

Experiences with 14 patients undergoing rupture of the left ventricle following mitral valve replacement over a period of 9 years have been described. Three different types have been recognized. Before 1978, most injuries occurred in the atrioventricular groove, apparently resulting from traction that insidiously avulsed the mitral annulus from the underlying left ventricular muscle. Several changes in operative technique, described in the text, were made to prevent this traction avulsion. Following the adoption of these principles, rupture in the atrioventricular groove virtually disappeared. A second type of injury, strut perforation, has been recognized in only one patient, a small 81-year-old female in whom the prosthesis inserted was too large for the ventricular cavity. Translucent obturators were subsequently developed not only to size the left ventricle but also to note the location of the post of the porcine prosthesis before insertion. Further problems of this type have not been seen. The most puzzling, and currently the most significant, problem is a third type of rupture, the mid-ventricular rupture, suggested as Type III by Miller in 1978 and described in detail by Cobbs in 1977 and 1980. The phenomenon seems to be a true spontaneous rupture of a thin left ventricle, usually occurring in small elderly women with mitral valve disease. If the friability of the left ventricle is transiently increased with potassium cardioplegia, such ventricles may spontaneously rupture following division of the chordae to the annulus of the mural leaflet. If this concept is correct, a rupture in some patients can best be prevented by preserving these chordae. It is well realized, of course, that a fortunate narrative experience of 3 1/2 years does not have any statistical value concerning a complication that occurs in 1 to 2% of operations. The experiences are reported, however, because to our knowledge, the untethered loop hypothesis has not been previously evaluated in a large number of consecutive patients operated on. Future comparison of experiences reported by others should make it possible to determine whether or not this concept is correct.

Acute myocardial infarction is complicated by cardiac rupture in 4% to 24% of all infarction deaths, and approximately 10% of hospital infarction deaths. There are no reliable indices to determine which patients run an increased risk of cardiac rupture. This report describes the surgical treatment and outcome of a patient who sustained a rupture of the left ventricular free wall, nine days after extensive anterior myocardial infarction.

In cardiac surgery significant residual lesions increase postoperative morbidity and mortality. Although intraoperative epicardial real-time two-dimensional Doppler echocardiography (two-dimensional Doppler) is an accurate and efficient technique for assessing the presence and severity of a residual lesion, it requires placement of a transducer in the operating field and consequent obstruction of the operative procedure. Transesophageal two-dimensional Doppler echocardiography (transesophageal two-dimensional Doppler), which can be applied intraoperatively and postoperatively without such problems, was performed in 35 patients during cardiac surgery (12 patients) and/or at an intensive care unit within 6 hr after cardiac surgery (30 patients). In those with constrictive pericarditis, an extensive pericardiectomy was performed with effective monitoring by intraoperative transesophageal two-dimensional Doppler. Abnormal posterior wall motion was observed in the case of left ventricular rupture (type III) after mitral valve replacement 3 hr before clinical manifestation. After prosthetic valve replacement (18 St. Jude Medical valves, one Carpentier-Edwards valve, one Björk-Shiley valve), no perivalvular leakage was detected, but minor physiologic transvalvular leakage was noticed in 11 patients with St. Jude Medical valves. In two patients with congenital heart disease, a small residual shunt was detected. In a patient in which a composite valve graft with direct coronary artery reattachment (Bentall's operation) was performed, reattachment was confirmed to be satisfactory. In conclusion, intraoperative and early postoperative monitoring of cardiac function by transesophageal two-dimensional Doppler echocardiography can improve the results of cardiovascular surgery by providing accurate information on cardiovascular structure and blood flow dynamics.

Thirteen patients who had ventricular septal defects (VSDs) after myocardial infarction (MI) underwent two-dimensional echocardiography (2-D echo), with confirmation of the VSD by oximetry. Eight of the patients were male and five were female, ages 51-76 years. Five had anterior and eight inferior MIs. Two-dimensional echocardiography revealed akinesis or dyskinesis of the interventricular septum (IVS) in all 13 patients. In only six could a defect in the IVS be directly visualized. Two-dimensional echocardiographic left ventricular (LV) wall motion abnormalities correlated with ECG and angiographic site of infarction in all patients. Twelve patients had adequate saline contrast studies. Positive LV contrast (microbubbles entering the left ventricle through the VSD) was seen in 11 patients, and negative right ventricular (RV) contrast (washout of the RV bubbles by LV blood crossing the VSD) in five patients; at least one abnormality was present in every patient. The location of the VSD was determined by visualizing a VSD or by the site of the positive LV or negative RV contrast. Oximetry showed VSD shunts of 1.4:1 to 7:1, with no correlation between the degree of negative RV contrast and shunt size. Surgical or pathologic confirmation of VSD was obtained in 12 patients, with agreement of VSD location by 2-D echo in all. Four of the 11 patients who underwent surgical repair died, and two patients died before surgery could be attempted. We conclude tht 2-D echo is a sensitive, rapid and safe technique for diagnosing VSD after MI. Positive LV contrast, with or without negative RV contrast, is more sensitive in the diagnosis and localization of post-MI VSD than direct echocardiographic visualization of the defect.

Over a 5.5 year period, 1264 consecutive patients with acute myocardial infarction as confirmed by enzyme levels were prospectively identified. Of these, 25 (2%) suffered ventricular septal rupture (pulmonary/systemic flow range 1.5 to 6) 7 +/- 7 days after onset of myocardial infarction. Death occurred in 14 patients (56%) and was more common after inferior than anterior myocardial infarction (11 of 15 [73%] vs three of 10 [30%], p less than .05). Among 133 variables analyzed, survivors and nonsurvivors were similar with respect to all premorbid clinical characteristics, infarct size as assessed by peak creatine kinase values, shunt size, two-dimensional echocardiographic and hemodynamic indexes of left ventricular function, and extent of coronary disease. Compared with survivors, the nonsurvivors had greater impairment of right ventricular function as determined by a higher two-dimensional echocardiographically derived right ventricular wall motion index (RVWMI) (0.55 +/- 0.87 vs 1.70 +/- 0.45, p less than .001), greater elevation of right ventricular end-diastolic pressure (11 +/- 6 vs 17 +/- 6, p less than .02), and greater mean right atrial pressure (10 +/- 6 vs 16 +/- 3, p less than .01). Of interest, two of the three patients who presented with anterior myocardial infarction and who died had inferiorly extended infarcts and all had abnormal RVWMIs (greater than or equal to 1.0). As expected, cardiogenic shock shortly after onset of ventricular septal rupture was associated with a 91% mortality, but was more common after inferior than anterior myocardial infarction (60% vs 20%, p less than .05). The mean effective cardiac index was also higher in survivors than nonsurvivors (2.1 +/- 0.5 vs 1.2 +/- 0.5, p less than .001). Finally, multivariate analysis indicated that all nonsurvivors could be identified based on: an effective cardiac index of 1.75 liters/min/m2 or less, the presence of extensive right ventricular and septal dysfunction on the two-dimensional echocardiogram, a mean right atrial pressure of 12 mm Hg or more, and early onset of ventricular septal rupture. Thus, our data demonstrate that: mortality is higher when ventricular septal rupture complicates inferior than when it complicates anterior myocardial infarction, survivors can be distinguished from nonsurvivors and the prediction of outcome is highly accurate, and combined right ventricular and septal dysfunction has a substantial impact on prognosis.