Acute myocardial infarction and cardiac arrest due to coronary artery perforation after mitral valve surgery: successful treatment with a covered stent.

We present a case of a gentleman who presented with acute myocardial infarction and cardiac arrest 6 days after undergoing mitral valve replacement surgery. Immediate coronary angiography revealed perforation of the left circumflex artery which was successfully treated with a covered stent. This report details the successful percutaneous treatment of an exceedingly rare complication of mitral valve surgery.

Wellens syndrome: a life-saving diagnosis.

The diagnosis of acute coronary syndrome relies on clinical history, electrocardiographic (ECG) changes, and cardiac biomarkers; but within the spectrum of acute coronary syndrome, there exist subtle presentations that cannot afford to be overlooked. Wellens syndrome is one such example, in which a patient can present with both ECG changes that are not classic for myocardial ischemia and negative cardiac biomarkers. The characteristic ECG findings associated with Wellens syndrome consist of deep, symmetric T-wave inversions in the anterior precordial leads. However, Wellens syndrome can also present as biphasic T-wave inversions in those same ECG leads. The associated critical stenosis of the proximal left anterior descending artery carries an immediately life-threatening prognosis if not recognized promptly (Am Heart J. 1982;103[4 Pt 2]:730-736). We describe a case of a less common manifestation of Wellens syndrome (type 1) followed by a discussion of its implications and management.

Sudden cardiac death due to large coronary aneurysm successfully treated with a covered stent and ChromaFlo guidance.

We present the case of a gentleman who presented to our hospital with recurrent episodes of sudden cardiac death treated initially with cardioversion. Immediate coronary angiography revealed a 7 mm aneurysm in the proximal left coronary artery. Using intravascular ultrasound and ChromaFlo technology, the aneurysm was successfully treated with a polytetrafluoroethylene-covered stent and the patient had no further episodes of sudden cardiac death.

Inaccuracy of Doppler echocardiographic estimates of pulmonary artery pressures in patients with pulmonary hypertension: implications for clinical practice.

BACKGROUND: Recent studies suggest that Doppler echocardiography (DE)-based estimates of pulmonary artery systolic pressure (PASP) may not be as accurate as previously believed. We sought to determine the accuracy of PASP measurements using DE compared with right-sided heart catheterization (RHC) in patients with pulmonary hypertension (PH). METHODS: We compared DE estimates of PASP to invasively measure PASP during RHC in 160 consecutive patients with PH (part one). To account for possible changes in hemodynamics between DE and RHC, we then prospectively determined PASP in an additional 23 consecutive patients undergoing simultaneous RHC and DE (part two). Bland-Altman analyses were performed to evaluate the agreement between RHC and DE measurements of PASP. Accuracy was predefined as 95% limits of agreement within ± 10 mm Hg for PASP estimates. RESULTS: In part one, there was moderate correlation between DE and RHC measurements of PASP (r = 0.68, P < .001). However, using Bland-Altman analysis, the bias for DE estimates of PASP was 2.2 mm Hg with 95% limits of agreement ranging from -34.2 to 38.6 mm Hg. DE estimates of PASP were determined to be inaccurate in 50.6% of patients. In part two, there was moderate correlation between DE and RHC measurements of PASP (r = 0.71, P < .01). However, despite simultaneous DE and RHC measurements, the bias for DE estimates of PASP was 8.0 mm Hg with 95% limits of agreement ranging from -28.4 to 44.4 mm Hg. CONCLUSIONS: DE estimates of PASP are inaccurate in patients with PH and should not be relied on to make the diagnosis of PH or to follow the efficacy of therapy.

Hypoplastic coronary artery disease: A rare cause of sudden cardiac death and its treatment with an implantable defibrillator.

A 21-year-old African American male presented to the emergency department after an episode of unexplained syncope. He had no significant past medical history. The initial physical examination was within normal limits, and his 12-lead electrocardiogram showed no signs of ischemia or evidence of chamber enlargement. The patient received a transthoracic echocardiogram which demonstrated mild global left ventricular dysfunction with an estimated ejection fraction of 45%. Coronary angiography was next performed and found no evidence of atherosclerotic coronary artery disease but did reveal hypoplasia of the left circumflex and right coronary arteries, with intraluminal diameters of approximately 1 mm. The left anterior descending coronary artery was small distally. Cardiac magnetic resonance imaging with gadolinium enhancement found no evidence of myocardial scar. The patient was ultimately diagnosed with aborted sudden cardiac death due to hypoplastic coronary artery disease (HCAD). The patient received an implantable cardioverter-defibrillator (ICD) prior to hospital discharge for secondary prevention of sudden cardiac death. One year after this presentation, the patient has been asymptomatic, with no ICD discharges.

Echocardiographic quantification of left ventricular mass: prognostic implications.

Left ventricular hypertrophy (LVH) has been shown to be an independent risk factor for adverse cardiac and cerebrovascular events. Despite this well-known association, the lack of a standardized approach for the quantification and the monitoring of LVH regression has limited its use as a primary risk factor that can be easily clinically targeted. Echocardiography has become the most widespread tool used for the quantification of LVH. With advances in this technology, echocardiographic quantification of LVH has improved and reference standards are being used to determine the clinical implications of LVH regression. In this article, we aim to provide a current appraisal of LVH with a focus on presenting the current clinical methods used to accurately detect LVH, the prognostic implications of these findings, and help develop a therapeutic target for clinicians.

Clinical methods for the detection and management of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) has been shown to be an independent risk factor for adverse cardiac and cerebrovascular events. Despite this well-known association, the lack of a standardized approach for both the quantification of LVH and the monitoring of LVH regression has limited its use as a primary risk factor that can be clinically targeted. In this State of the Art Paper, we will provide a current appraisal of LVH with a focus on presenting the current methods to accurately detect LVH and management strategies to develop a therapeutic target for clinicians.

Short duration exercise increases breath hydrogen excretion after lactulose ingestion: description of a new phenomenon.

OBJECTIVE: There is limited information on the effect of exercise on colonic function. Beneficial effects have been described, including prevention of colon cancer. In the present study, we demonstrate that short duration exercise results in enhancement of breath hydrogen excretion after consumption of lactulose. METHODS: Twelve normal volunteers who performed regular exercise were recruited. Each study subject underwent four study sessions (two resting and two exercise) after consumption of 10 g of crystalline lactulose. Colonic hydrogen production was measured in mid-expiratory breath samples obtained at baseline and frequent intervals to 420 min. Exercise sessions consisted of 5 min on a treadmill at a 20% incline at 10 km/h. This was performed 180 min after lactulose ingestion in the two exercise sessions. RESULTS: A characteristic pattern in the hydrogen concentration versus time curves was seen after exercises, consisting of an initial decrease then an increase in concentration above baseline for up to 3 h. Mean area under the curve from 0 to 420 min for resting studies was 5,156 +/- 2,621 ppm/min and was 7,051 +/- 2,447 ppm/min for exercise studies, p < 0.05 (37% increase). Mean area under the curve from 180 to 420 min was 2,808 +/- 1,592 ppm/min for resting studies and 4,543 +/- 1,729 for exercise studies, p < 0.005 (62% increase). CONCLUSION: This study demonstrates that exercise potentially enhances the metabolism of lactulose by colonic bacteria. The authors postulate that this effect is due to stirring of the colonic contents. The described phenomenon may explain, in part, the beneficial effects of exercise on colonic mucosa.