Acquired long QT syndrome from stress cardiomyopathy is associated with ventricular arrhythmias and torsades de pointes.

BACKGROUND: Stress cardiomyopathy (SCM) is a syndrome of transient ventricular dysfunction triggered by severe emotional or physical stress, likely resulting from catecholamine-mediated myocardial toxicity. Repolarization abnormalities associated with other hyperadrenergic states can cause QT prolongation and lethal arrhythmia including torsades de pointes (TdP). Despite the development of repolarization abnormalities and QT prolongation in SCM, little is known about the risk of ventricular fibrillation (VF) and TdP. OBJECTIVE: The aim of this study was to assess the prevalence and clinical predictors of ventricular arrhythmias in a cohort of patients with SCM. METHODS: Data from a registry of consecutive patients with SCM from 2 institutions were reviewed. Patients who developed VF or TdP were identified. Clinical characteristics and outcomes were analyzed and compared with a control group of patients with SCM without VF/TdP. RESULTS: Of 93 patients with SCM, 8 (8.6%) experienced VF/TdP. Of these 8 patients, 2 presented with VF and were subsequently diagnosed with SCM. Six other patients experienced pause-dependent TdP or VF after SCM diagnosis in the setting of substantial QT prolongation. Prolongation of the corrected QT interval (QTc) was significantly associated with the occurrence of ventricular arrhythmia (odds ratio 1.28 for each 10 ms increase in QTc, 95% confidence interval 1.10 to 1.50). CONCLUSION: SCM can be associated with life-threatening ventricular arrhythmia in over 8% of cases. SCM should be recognized among the causes of acquired long QT syndrome and can be associated with a risk of TdP.

Prevalence and clinical characteristics of right ventricular dysfunction in transient stress cardiomyopathy.

Transient stress cardiomyopathy (TSC) is a cause of reversible left ventricular (LV) dysfunction that is increasingly recognized. Reports to date have focused primarily on LV involvement, with little attention paid to associated right ventricular (RV) dysfunction. With other forms of LV dysfunction, RV involvement has been shown to confer an adverse prognosis. Prevalence, clinical characteristics, and short-term prognosis of RV dysfunction in TSC remain ill-defined. Presenting echocardiograms of 40 patients with TSC were reviewed. RV function was assessed by evaluating regional wall motion and calculating a wall motion score index (WMSI). RV dysfunction was defined as a WMSI >1.0. Clinical and demographic characteristics of patients with and without RV dysfunction were compared. RV dysfunction was identified in 27% of patients (11 of 40). RV WMSI was 1.20 +/- 0.30 for the entire cohort compared with 1.72 +/- 0.30 for those with RV dysfunction (p <0.05). In each case with RV dysfunction, regional wall motion abnormalities involved the apex and spared the base. Patients with RV dysfunction had higher B-type natriuretic peptide levels, higher pulmonary artery systolic pressures, and longer hospital stays. RV dimensions, clinical characteristics, electrocardiographic findings, other biomarkers, and in-hospital complications were similar. In conclusion, RV wall motion abnormalities, predominantly involving the apex and sparing the base, occur in slightly >1/4 of cases of TSC. Although associated with higher B-type natriuretic peptide levels, higher pulmonary artery systolic pressures, and longer hospital stays, RV dysfunction was not associated with significant differences in short-term cardiac morbidity or increased early mortality.

Usefulness of the pulmonary arterial systolic pressure to predict pulmonary arterial wedge pressure in patients with normal left ventricular systolic function.

Tissue Doppler imaging combined with transmitral Doppler permits estimation of pulmonary artery wedge pressure (PAWP) in many, but not all, patients, whereas pulmonary artery systolic pressure (PASP) and cardiac output (time-velocity integral method) are routinely measured. It was hypothesized that simple Doppler echocardiographic measurements could be used to estimate PAWP in many patients by rearranging the equation for pulmonary vascular resistance ([mean pulmonary artery pressure - (left atrial pressure/cardiac output)] x 80). Data from 69 patients (mean age 59 +/- 15 years) were reviewed, including cardiac output, transmitral mitral E wave velocity, and lateral tissue Doppler imaging mitral annular early diastolic velocity. PAWP was determined in the 2 ways of (1) measured (PAWPm) using the regression equation PAWPm = 1.91 + (1.24 * transmitral mitral E wave velocity/mitral annular early diastolic velocity) developed and validated by Nagueh, and (2) using a nomogram that we developed to predict PAWP when cardiac output and PASP were known. Moderately strong correlation was found between PASP and PAWPm (r = 0.73), and this correlation improved when excluding patients with pulmonary or liver disease and restricting cardiac output to 3.5 to 6.0 L/min (physiologic range; r = 0.81). Furthermore, the relation between PAWPm and PASP allowed for discrimination of high versus low PAWP: 36 of 37 patients with PASP < or =30 mm Hg had PAWPm < or =15 mm Hg (sensitivity 97%, specificity 47%). Conversely, 9 of 9 patients with PASP > or =40 mm Hg had PAWPm > or =12 mm Hg (sensitivity 100%, specificity 70%). Predicted PAWP correlated well with PAWPm (r = 0.63) and improved when patients with liver or pulmonary disease were excluded (r = 0.83). In conclusion, PASP strongly correlated with PAWP, and this principle can be exploited to rapidly detect patients with low or high PAWP.

Heart failure in the "oldest old": clinical and echocardiographic insights.

While the incidence and prevalence of heart failure (HF) increase markedly with age, few studies have included data on a large series of patients aged 85 years and older. Clinical and echocardiographic data from 533 patients admitted to a tertiary care hospital for acute HF were obtained. Data from the oldest old (>or=85 years; n=252; mean age, 91.9+/-3.6 years) were compared with data from those aged 65 to 74 years (n=123; mean age, 70.1+/-2.8 years) and 75 to 84 years (n=158; mean age, 79.4+/-2.9 years). Echocardiographic data were consistent with hypertensive remodeling. The proportion of patients with HF and a preserved left ventricular ejection fraction was greatest in the oldest patients (61%) in comparison to patients aged 65 to 74 years (48%) and 75 to 84 years (48%). Approximately three-fourths of the oldest patients were women, and two-thirds of women had a left ventricular ejection fraction >or=50%.