Multiple Recurrent Infective Endocarditis Secondary to Streptococcus mitis Bacteremia Despite Proper Antibiotic and Surgical Treatment.

Infective endocarditis (IE) is a rare and potentially fatal disease. It is an infection of the endocardium of the heart and heart valves. One of the major complications faced by patients who have recovered from a first episode of IE is recurrent IE. Risk factors for recurrent IE include intravenous (IV) drug use, prior episodes of IE, poor dentition, recent dental procedures, male gender, age over 65, prosthetic heart valve endocarditis, chronic dialysis, positive valve culture(s) obtained at the time of surgical intervention, and persistent postoperative fever. We present a case of a 40-year-old male with a history of former IV heroin use who experienced multiple episodes of recurrent IE caused by the same pathogen, Streptococcus mitis. This recurrence occurred despite the patient completing the appropriate course of antibiotic therapy, undergoing valvular replacement, and maintaining drug abstinence for two years. This case highlights the challenges associated with identifying the source of infection and emphasizes the need to develop guidelines for surveillance and prophylaxis against recurrent IE.

A Pressing Matter: Compressive Postoperative Hematoma Causing Acute Diastolic Heart Failure.

BACKGROUND: Cardiopulmonary complications in the postoperative period can lead to significant morbidity and mortality. Many of the complications in the postoperative period occur after discharge from the hospital, and up to 25% of patients will require readmission. In postoperative patients presenting to the emergency department (ED), it is important to consider that postoperative complications can affect a multitude of organ systems, including those that are adjacent to where the surgery was performed. CASE REPORT: We present the case of a 54-year-old woman presenting to the ED with shortness of breath in the setting of recent Nissen fundoplication revision. Pulmonary angiography was significant for a large hiatal hernia and negative for pulmonary embolism. She was discharged and returned to the ED a few days later due to worsening symptoms. Further diagnostic studies demonstrated an esophageal hematoma causing compression of the left atrium, leading to acute diastolic heart failure. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: It is important to consider alternative etiologies for common complaints in the postoperative patient presenting to the ED. Early involvement of the operative team in the patient's care can assist in directing diagnostic approach and management of the postoperative patient.

The use of contrast echocardiography in the diagnosis of an unusual cause of congestive heart failure: achalasia.

Extrinsic compression of the left atrium is a potentially life-threatening but unusual cause of congestive heart failure. Achalasia is a motility disorder characterized by impaired relaxation of the lower esophageal sphincter and dilation of the distal two-thirds of the esophagus. We report only the third known case in the world literature of massive left atrial compression by a dilated esophagus in a patient with achalasia. The use of contrast echocardiography with perflutren protein-type A microspheres allowed for differentiation between a compressive vascular structure and the esophagus. This resulted in prompt treatment leading to hemodynamic stability after nasogastric decompression and Botulinum toxin injection at the gastroesophageal junction.

Case report: Acute myocardial infarction in a 32-year-old white male found to have antiphospholipid antibody syndrome and MTHFR mutation homozygosity.

We report the diagnosis and management of a 32-year-old Hungarian male, whose only known risk factor for coronary artery disease was smoking, who presented with an acute thrombotic anterolateral wall myocardial infarction requiring percutaneous transluminal coronary angioplasty (PTCA) stenting of his proximal left anterior descending coronary artery. He arrived to the emergency room with an abnormally prolonged partial thromboplastin time (PTT) that subsequently did not correct by mixing with normal plasma. This was suggestive of an underlying coagulopathy. An extensive coagulopathy work up found him to have the antiphospholipid antibody syndrome with antibodies positive for anticardiolipin, lupus anticoagulant and false-positive VDRL. Genetic typing found him to be homozygous for a mutation in the methylenetetrahydrofolate reductase (MTHFR A1298C) gene, which, in the presence of additional thrombophilic factors, may have increased his risk of myocardial infarction. He was discharged on high dose coumadin.

Preservation of myocardial microcirculation during mechanical reperfusion for myocardial ischemia with either abciximab or eptifibatide.

Myocardial Blush Grade (MBG) is an angiographic method of assessing myocardial microcirculation and provides independent risk stratification among patients with normal TIMI 3 flow. Although the beneficial effect of abciximab on microvascular perfusion is well established, the efficacy of eptifibatide in the prevention of platelet aggregation and distal microembolization is less proven. After a pharmacologic shift by our institution towards the use of eptifibatide in patients with unstable angina presenting for PCI, we sought to evaluate our experience by retrospectively comparing the effect on myocardial perfusion between abciximab and eptifibatide following PCI in stable angina or acute coronary syndrome. Microcirculatory perfusion was reviewed in 101 consecutive patients (23 stable angina, 61 unstable angina, 17 non-q MI) undergoing PTCA/stenting. This comparison was between the last group of 51 patients who routinely received standard bolus and infusion of abciximab and the first group of 50 patients who began receiving standard bolus and infusion of eptifibatide. Baseline characteristics between the two groups were balanced, except for more patients with previous CABG in the eptifibatide group. Angiograms were evaluated by 2 blinded independent reviewers for MBG as follows: 0, no blush; 1, minimal blush; 2, moderate blush; and 3, normal blush. TIMI 3 flow was seen in 98 patients. MBG scores were not significantly different in the abciximab group (67% MBG 3; 31% MBG 2; 2.0% MBG 0 1) than in the eptifibatide group (58% MBG 3; 36% MBG 2; 6.0% MBG 0 1); p = 0.34. Patients with prior PTCA/stenting had lower MBG scores (0 2) compared to patients without prior PTCA (58% vs 31%; p = 0.03). There were significantly lower MBG scores in all patients with prior PTCA or CABG compared to patients without (55% vs 30%; p = 0.03). MBG scores significantly and inversely correlated with peak troponin I levels (r = -0.18, one-tailed p = 0.04). The similarity in myocardial perfusion between abciximab and eptifibatide suggests that both compounds are equally effective in reducing platelet aggregation and microembolization during mechanical reperfusion. Lower MBG scores in patients with prior PTCA or revascularization may be explained by irreversible microvascular dysfunction resulting from distal microembolization during the previous procedure. Lower MBG scores in patients with higher troponin I levels may reflect more frequent microemboli and microinfarcts during an ischemic event. Larger prospective studies need to be performed to validate these findings.

Natriuretic peptides: biochemistry, physiology, and therapeutic role in heart failure.

Cardiac natriuretic peptides are a family of structurally related peptides that are important in sodium and volume homeostasis. They consist of atrial natriuretic peptide, brain natriuretic peptide, and C-type natriuretic peptide and are elevated in patients with left ventricular dysfunction. In contrast with vasoconstrictive hormones, such as norepinephrine, angiotensin II, and arginine vasopressin, which worsen the physiological milieu in patients with left ventricular dysfunction and heart failure, the natriuretic peptides ameliorate these effects by promoting natriuresis, diuresis, peripheral vasodilation, and by inhibiting the renin-angiotensin system. The serum levels of the natriuretic peptides correlate with the severity of heart failure and appear to have prognostic value. The present article reviews the biochemistry, molecular biology, and physiology of natriuretic peptides and their pathophysiological link to heart failure. The therapeutic uses of natriuretic peptides are also reviewed. This includes the use of intravenous nesiritide, a synthetic human brain natriuretic peptide, and the recently developed vasopeptidase inhibitors which are designed to inhibit the degradation of natriuretic peptides.