Throws of Death: Traumatic Coronary Artery Dissection Resulting From Jiu Jitsu Training.

BACKGROUND: The risk of cardiac injury in blunt thoracic trauma is quite rare, occurring in only 0.1% of patients. The least common cardiac injury is coronary artery dissection. Most cardiac injuries result from high-energy mechanisms such as motor vehicle collisions. Even low-mechanism injuries that have been reported involved rapid deceleration. CASE REPORT: We present a case of traumatic coronary artery dissection that resulted from a low-energy blunt thoracic injury with no rapid deceleration. This patient had no other associated thoracic injuries, such as rib fractures or sternal fracture. Following presentation, our patient twice deteriorated into ventricular fibrillation and was successfully resuscitated each time. The coronary lesion was successfully stented and the patient was eventually discharged home. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: This case underscores the importance of maintaining a high level of suspicion for coronary artery dissection even in low-energy mechanisms. An electrocardiogram should be obtained early, even in low-energy mechanisms. While patients with traumatic cardiac injuries will commonly present with other injuries, such as rib fractures, the absence of these injuries does not rule out cardiac injury.

Changes in ventricular remodelling and clinical status during the year following a single administration of stromal cell-derived factor-1 non-viral gene therapy in chronic ischaemic heart failure patients: the STOP-HF randomized Phase II trial.

BACKGROUND: Stromal cell-derived factor-1 (SDF-1) promotes tissue repair through mechanisms of cell survival, endogenous stem cell recruitment, and vasculogenesis. Stromal Cell-Derived Factor-1 Plasmid Treatment for Patients with Heart Failure (STOP-HF) is a Phase II, double-blind, randomized, placebo-controlled trial to evaluate safety and efficacy of a single treatment of plasmid stromal cell-derived factor-1 (pSDF-1) delivered via endomyocardial injection to patients with ischaemic heart failure (IHF). METHODS: Ninety-three subjects with IHF on stable guideline-based medical therapy and left ventricular ejection fraction (LVEF) ≤40%, completed Minnesota Living with Heart Failure Questionnaire (MLWHFQ) and 6-min walk distance (6 MWD), were randomized 1 : 1 : 1 to receive a single treatment of either a 15 or 30 mg dose of pSDF-1 or placebo via endomyocardial injections. Safety and efficacy parameters were assessed at 4 and 12 months after injection. Left ventricular functional and structural measures were assessed by contrast echocardiography and quantified by a blinded independent core laboratory. Stromal Cell-Derived Factor-1 Plasmid Treatment for Patients with Heart Failure was powered based on change in 6 MWD and MLWHFQ at 4 months. RESULTS: Subject profiles at baseline were (mean ± SD): age 65 ± 9 years, LVEF 28 ± 7%, left ventricular end-systolic volume (LVESV) 167 ± 66 mL, N-terminal pro brain natriuretic peptide (BNP) (NTproBNP) 1120 ± 1084 pg/mL, MLWHFQ 50 ± 20 points, and 6 MWD 289 ± 99 m. Patients were 11 ± 9 years post most recent myocardial infarction. Study injections were delivered without serious adverse events in all subjects. Sixty-two patients received drug with no unanticipated serious product-related adverse events. The primary endpoint was a composite of change in 6 MWD and MLWHFQ from baseline to 4 months follow-up. The primary endpoint was not met (P = 0.89). For the patients treated with pSDF-1, there was a trend toward an improvement in LVEF at 12 months (placebo vs. 15 mg vs. 30 mg ΔLVEF: -2 vs. -0.5 vs. 1.5%, P = 0.20). A pre-specified analysis of the effects of pSDF-1 based on tertiles of LVEF at entry revealed improvements in EF and LVESV from lowest-to-highest LVEF. Patients in the first tertile of EF (<26%) that received 30 mg of pSDF-1 demonstrated a 7% increase in EF compared with a 4% decrease in placebo (ΔLVEF = 11%, P = 0.01) at 12 months. There was also a trend towards improvement in LVESV, with treated patients demonstrating an 18.5 mL decrease compared with a 15 mL increase for placebo at 12 months (ΔLVESV = 33.5 mL, P = 0.12). The change in end-diastolic and end-systolic volume equated to a 14 mL increase in stroke volume in the patients treated with 30 mg of pSDF-1 compared with a decrease of -11 mL in the placebo group (ΔSV = 25 mL, P = 0.09). In addition, the 30 mg-treated cohort exhibited a trend towards improvement in NTproBNP compared with placebo at 12 months (-784 pg/mL, P = 0.23). CONCLUSIONS: The blinded placebo-controlled STOP-HF trial demonstrated the safety of a single endocardial administration of pSDF-1 but failed to demonstrate its primary endpoint of improved composite score at 4 months after treatment. Through a pre-specified analysis the STOP-HF trial demonstrates the potential for attenuating LV remodelling and improving EF in high-risk ischaemic cardiomyopathy. The safety profile supports repeat dosing with pSDF-1 and the degree of left ventricular remodelling suggests the potential for improved outcomes in larger future trials.

Stem cell therapy for heart disease.

Coronary artery disease is the leading cause of death in Americans. After myocardial infarction, significant ventricular damage persists despite timely reperfusion and pharmacological management. Treatment is limited, as current modalities do not cure this damage. In the past decade, stem cell therapy has emerged as a promising therapeutic solution to restore myocardial function. Clinical trials have demonstrated safety and beneficial effects in patients suffering from acute myocardial infarction, heart failure, and dilated cardiomyopathy. These benefits include improved ventricular function, increased ejection fraction, and decreased infarct size. Mechanisms of therapy are still not clearly understood. However, it is believed that paracrine factors, including stromal cell-derived factor-1, contribute significantly to stem cell benefits. The purpose of this article is to provide medical professionals with an overview on stem cell therapy for the heart and to discuss potential future directions.

Acute Myocardial Infarction and Stress Cardiomyopathy Are Not Mutually Exclusive.

BACKGROUND: Stress cardiomyopathy is a transient cardiac syndrome characterized by reversible left ventricular systolic dysfunction precipitated by emotional or physiologic stress. The presence of obstructive coronary artery disease has been noted in stress cardiomyopathy. METHODS: We describe 3 case reports of patients with acute coronary syndrome and transient wall motion abnormalities not usually seen in the distribution of coronary artery disease. RESULTS: In these 3 cases of acute myocardial infarction, the distribution of the culprit coronary occlusion was not concordant with the territory of transient wall motion abnormality. Follow-up demonstrated resolution of the wall motion abnormalities without intervention in these territories. CONCLUSION: We believe that the physiologic stress of the acute coronary syndrome may have precipitated the stress cardiomyopathy as presented by these patients. This is the first demonstration that stress cardiomyopathy may be precipitated by acute coronary syndrome.

Shortness of breath, syncope, and cardiac arrest caused by systemic mastocytosis.

During a 3-month period, a 33-year-old man presented to the emergency department on 4 occasions with dyspnea, palpitations, and syncope. His initial presentation was accompanied by acute myocardial injury and ventricular fibrillation. An extensive evaluation spanned the 3 months and included echocardiography, cardiac catheterization, electrophysiology study, tilt-table evaluation, pulmonary angiography, electroencephalography, and serum and urine analysis. Diagnosis eluded clinicians until a rash was recognized to be urticaria pigmentosa, and biopsy of the rash then implicated mastocytosis. Since the initiation of pharmacotherapy nearly 5 years ago, the patient has remained asymptomatic. This case demonstrates that systemic mastocytosis can present as recurrent syncope and even as cardiac arrest. Diagnosis of this rare but potentially fatal disease is made particularly challenging by its protean manifestations.

Dual-catheter covered stenting: a novel approach to the treatment of large coronary artery perforations.

Coronary perforation is an infrequent but potentially devastating complication of coronary intervention. Treatment of a broad-based perforation usually requires emergent pericardiocentesis and thoracotomy. We present a novel approach to closure of > or = 1 mm diameter perforations using a dual-catheter covered stent technique.