Dalal B, MD; Dalal I, MD; Shah U, MD; Dalal P, MD; Nasser K, MD; Dalal SB, MD
V. S. General Hospital, India, Sinai-Grace Hospital/Wayne State University, Detroit, MI.
Introduction
Despite the rise in occurrence, echinococcosis remains a very rare disease (<1 case per 1 million inhabitants) in the continental United States. Northern Alaska has endemic areas of E granulosus.
60% of the hydatid cysts are found in liver, 30% in lungs, 2.5% in kidney, 2.5% in heart and pericardium and 5% in other areas. We are reporting a case report of multiple hydatid cysts in heart.
Case report
A 30 year old male came to the out patient clinic with complaints of intermittent chest pain & palpitations. Physical examination was normal except PMI was displaced laterally. EKG was showing RVH with RBBB. 2D echo showed multiple well defined cystic lesions with presence of daughter cysts, the appearance compatible with Hydatid Cyst. Doppler showed mild to moderate MR. USG of the abdomen was normal. Patient underwent for open heart surgery and all the cysts were removed. Patient was also prescribed Albendazole (400 mg twice a day) for period of 12 weeks. Postoperative 2D Echo didn’t reveal any cyst. Subsequently patient didn’t have complains of chest pain or palpitation.
Discussion
Cardiac involvement of hydatid cyst is rare though, solitary hydatid cyst of heart is well documented. In our patient there were multiple cysts in heart with predominance in RV and IVS. In spite of that he was minimally symptomatic and such symptoms are always overlooked by the patient as well as physicians. Diagnosis of hydatid cyst in heart can be easily made by 2D echo. CT scan or MRI may help for lesions with mixed echogenic pattern on echocardiography. Casoni’s test, complement fixation, indirect haemagglutination, latex agglutination and indirect fluorescent antibody tests are used to make diagnosis. Cysts excision is the mainstay of treatment. If untreated, hydaitd cyst of heart can cause arrhythmia, syncope, rupture of cyst in heart. Albendazole or Mabendazole is given to sterilize the cyst and to prevent recurrence if spillage occurred during surgery. Public education is essential to prevent echinococcosis.
HEMOLYTIC ANEMIA AFTER MITRAL VALVE REPAIR
Zainab Shahid, MD, Anjali Gupta, MD, Tannu Sahay, MD, Joel Appel, DO,
FACP.
Department of Internal Medicine, Sinai-Grace
Hospital/Detroit Medical Center, Wayne State University, Detroit, Michigan.
Introduction: Microangiopathic hemolytic anemia is commonly seen
after mitral valve replacement. But it is an uncommon complication of mitral
valve repair and is considered a failure of the valve repair. We present a case
of hemolysis after mitral valve repair.
Case
Report: A 54-year-old hypertensive
and diabetic male presented with progressive exertional dyspnea, chest pain and
dark colored urine. Patient had undergone Mitral Valve repair one month earlier
for severe mitral regurgitation. Past medical history was also significant for
Hodgkin's disease in remission and prostate cancer. Lab results showed
normocytic anemia with reticulocytosis, indirect bilirubinemia, elevated LDH
(2296 U/l), low haptoglobin<6mg/dl, negative Coombs test, increased serum
creatinine (3 mg/dl) and
hematuria. The peripheral smear showed schistocytes and polychromasia.
Transthoracic echocardiography was done, showing moderate to severe mitral
regurgitation .No other cause of hemolysis was identified. Patient underwent
reoperation, approximately 3 weeks after presentation, showing dehiscence of
the annuloplasty ring with paravalvular leak. The valve was replaced by
St.Jude’s prosthetic valve. The patient recovered from the surgery without
complication and hemolysis resolved.
Discussion
and Conclusion: This case is a
unique presentation of early mitral valve repair failure. In the English
literature 65 such cases have been reported showing development of hemolysis
within 3-4 months. Hemolysis after valve repair is attributed to hydrodynamic
patterns associated with high shear stresses (fragmentation, collision, rapid
acceleration) and low shear stress (free jet and slow deceleration). The
mechanism in our patient was perceived as fragmentation of red blood cells due
to regurgitant jets against dehisced annuloplasty ring. In patients with signs
and symptoms of worsening CHF with low hemoglobin who have recently undergone
mitral valve repair, hemolytic anemia should be considered in the differential
diagnosis. The usual treatment is re-operation with mitral valve replacement.
Hemodynamic
and Clinical Changes in Patients Following Alcohol Septal Ablation for
Hypertrophic Obstructive Cardiomyopathy
Irfan Hameed,
MD, Amr Abbas, MD, Stacy Brewington, MD, Judy Boura, William O’Neil, MD, Sinai
Grace Hospital and William Beaumont Hospital, Michigan
Background:
Dynamic left ventricular outflow tract obstruction is an important determinant of patient’s symptoms and prognosis. Relief of outflow obstruction leads to positive clinical and hemodynamic effects. Alcohol Septal Ablation (ASA) is a reliable alternative to surgical myomectomy in symptomatic patients with Hypertrophic Cardiomyopathy (HCM) who fail medical therapy. We sought to determine the clinical and hemodynamic benefits following the procedure.
Methods:
A retrospective analysis of 40 patients who underwent ASA for HCM from 1999 to 2004 was conducted. Baseline clinical and echocardiographic findings were reviewed and compared at follow up. The changes from baseline to follow-up were compared using a chi-square or fisher's exact test. The differences were tested using a paired t-test. A p<0.05 was considered significant.
Results:
The mean age was 52 with 63% male. Median clinical follow up was 80 days and echocardiographic follow up was 46 days.
Clinically, a sustained improvement was noted in NYHA class, chest pain, palpitation, syncope, and use of medications. The majority of patients were NYHA class 3-4 at baseline (86%) and improved to class 1 (26%) at follow up, seventy percent of patients had no symptoms. Similarly, by echo an improvement in septal thickness (from 2.2 ± 0.6 to 1.6 ± 0.4 cm, P<0.0019), mitral regurgitation (from 96% to 58%, P< 0.039), and outflow gradient (from 74.0 ± 46 to 29 ± 33 mm Hg, P<0.0004) was noted.
Conclusion:
ASA leads to a hemodynamic and clinical improvement in patients with HCM.
Cardiac Sarcoidosis Presenting as Acute Non-ST Elevation
Myocardial Infarction
Ashraf Ahmed, M.D; Kamal Nasser, MD; Shazia Essani, MD
Department of Internal Medicine, Sinai-Grace Hospital, Detroit Medical Center, Detroit, MI
Background: Significant cardiac involvement in sarcoidosis occurs in 5% of patients, manifesting as sudden death, arrhythmia, conduction disorder, heart failure or cardiomyopathy. To date, this is the first reported case of cardiac sarcoidosis presenting with acute non-ST elevation myocardial infarction (MI).
Case Report: 68 years old African American female nonsmoker with a history of paroxysmal atrial fibrillation and first degree atrioventricular (AV) block, had severe shortness of breath at rest, wheezing, and dry cough for one day. She denied chest pain or history of bronchial asthma. On exam, she was in severe respiratory distress, using the accessory muscles of respiration, with bilateral decreased air entry, wheezes and prolonged expiratory phase. Cardiovascular exam was normal. EKG showed first-degree AV block without ischemic changes. Chest x-ray showed slight haziness and congestion. Patient initially improved with breathing treatments, but later she developed chest pain and troponins turned to be positive. She deteriorated significantly, requiring intraaortic balloon and a cardiac catheterization that showed occlusion of left anterior descending artery (LAD 75%), right coronary artery (RCA 100%), and circumflex artery (80%), with ejection fraction of 20% (decreased from 60%, four month prior to presentation). Emergency coronary bypass surgery revealed widespread epicardial involvement, including LAD, RCA, and circumflex artery, with noncaseating granuloma. Patient received oral steroids and an implantable defibrillator was placed.
Discussion: Sarcoidosis is a multisystem granulomatous disorder of unknown etiology. It has 5% mortality rate secondary to respiratory failure and cardiac involvement. Cardiac sarcoidosis commonly presents as conduction abnormalities, intractable arrhythmias (which can lead to sudden death), congestive heart failure and progressive cardiomyopathy which might require cardiopulmonary transplants. Corticosteroids remain the main therapy. The survival rate varies between 44 to 75 % at 5 years, among steroid treated patients.
Conclusion: It is very unusual for cardiac sarcoidosis to present as non-ST elevation MI. The mortality in cardiac sarcoidosis with infiltration of the coronaries is not established, as there are no similar cases reported in the literature.
Efficacy of Transcutaneous Pacing in Asystole
S. Rajaguru MD, S. Marur MD, Department of Medicine, Sinai Grace Hospital/ Wayne state University, Detroit, MI
Background: Asystole is the absence of electrical activity in the myocardium. Confirmation of the rhythm is crucial in the management of Asystole. Transcutaneous pacing (TCP) is the electrical stimulation from pads placed on the body to stimulate heart contraction. This is indicated as an emergency temporary solution to improve asystole, a slow heart rate with inadequate cardiac output. The aim of this study is to identify the efficacy of transcutaneous pacing in Asystole management.
Method: Extensive literature search was carried out on the studies done on asystole from 1980 onwards. Ovid and Pub med search were done using asystole and transcutaneous pacing as keywords. Selection criteria were randomized controlled prospective studies with reasonable number of population. Six studies were selected based on the selection criteria.
Results: Three out of these studies were done in the emergency department and the other three studies were carried out in pre-hospital settings. All the studies done in pre-hospital setting came to a similar conclusion.
Conclusion: Out of hospital studies concluded that transcutaneous pacing does not improve the survival of the patient with asystolyic cardiac arrest. In-hospital studies basically concluded that TCP should be done early enough to have a satisfactory out come.
Discussion: Asystole occurs due to several underlying conditions. However, the studies done so far have not taken etiology in to consideration. Here we suggest designing a retrospective study conducting on inpatients that develop asystolic cardiac arrest and received TCP as a study group. The control group will be the patients who develop asystolic cardiac arrest but did not receive TCP. Further more this study will analyse the out come considering underlying condition which can be obtained from the medical records.
What is the Risk for Thromboembolic Phenomenon in a
Patient with Dilated Cardiomyopathy?
Anna Trostinskaia MD, Department of Internal Medicine, Sinai-Grace Hospital, Wayne State University, Detroit
Patients with Dilated Cardiomyopathy (DC) have multiple factors that predispose them to thromboembolic (TE) events.
What is the risk of TE phenomenon in patients with DC? Medline/Pubmed/Ovid search of published studies was performed to find statistical data to analyze TE in DC patients. Seven small studies (5 retrospective and 2 prospective) and secondary analysis of 4 large prospective randomized trials were identified. None of randomized controlled studies evaluated TE events as a primary end point.
Prevalence and incidence of TE events (stroke, systemic and pulmonary emboli) in patients with CHF due to DC varied widely from study to study with the prevalence range 3 – 50% and incidence range 1.5 -3.5 / 100pt-years. One of the most significant confounders for TE risk evaluation in DC patients appeared to be nonrheumatic atrial fibrillation (AFib) (Crawford et all, 2004). One small study showed similar prevalence of TE events and mortality in patients with and without AFib (Polic et all, 1997).
Another large study which included only patients in normal sinus rhythm has shown significantly increased risk for TE events in women compared with men (2.4/100 patient-years and 1.8/100 patient-years respectively) (Koniaris et all,1998). Moreover, risk of stroke appeared to be left ventricular ejection fraction (LVEF) dependent in women but not in men and each 10% decline in LVEF was significantly associated with 53% increased risk of TE in women.
Other large studies demonstrated inversed correlation between TE events risk and LVEF without gender differences (Sirajuddin et all, 2002).
Conclusions: 1. The risk of TE events in patients with DC is poorly defined.
2. Studies of TE events risk in DC imply most important question to answer: Should all the patients with DC/CHF be anticoagulated?
3. Assuming insufficient data about TE events risk in patients with DC long term warfarin therapy can not be recommended until data are available from new upcoming trials. Presently, the only supported indications for anticoagulation in patients with DC are Afib, prior TE event, or Left Ventricular thrombus documented on imaging studies.