Determinants of atrial fibrillation development in patients with hypertrophic cardiomyopathy.

Predictors of the development of atrial fibrillation (AF) in patients who have hypertrophic cardiomyopathy (HC) have not been extensively studied, although, in these patients, AF contributes to the exacerbation of symptoms and the development of heart failure. The present study determined the role of left atrial (LA) function in the development of AF in patients who have HC. One hundred fifty consecutive patients who had HC, had no history of AF, and who were followed for 5.2 +/- 2.9 years constituted the study population. Using M-mode echocardiography, we measured LA function as global LA fractional shortening and LA diameter. LA volume was measured from 2-dimensional 4-chamber views by the method of disks. During follow-up, 20 patients developed AF. LA function was an independent predictor of AF (odds ratio 0.716, p = <0.001), whereas LA diameter and volume were predictors in addition to age. Kaplan-Meier analysis showed that LA dysfunction carried a high risk of AF. Thus, in patients who have HC, LA function is a strong predictor of AF development and is independent of age.

Dobutamine stress echocardiography in hypertrophic cardiomyopathy.

AIMS: Myocardial ischemia in the absence of coronary artery disease is common in patients with hypertrophic cardiomyopathy (HCM). Dobutamine stress echocardiography (DSE) induces left ventricular (LV) new wall motion abnormalities (NWMA) in some patients with HCM. We evaluated the effects of dobutamine on LV performance and hemodynamics in HCM. METHODS AND RESULTS: Eighteen patients with non-obstructive HCM underwent DSE. Dobutamine was administered at dosages of 5, 10, 20, 30 and 40 microg/kg/min with increments at intervals of 3 min. Seven patients developed NWMA, whereas the other 11 did not. During DSE, heart rate increased significantly more in NWMA patients,whereas LV outflow tract gradient (OTG) increased significantly and similarly in both groups. At peak dobutamine dose, NWMA patients had a significant increase in LV end-systolic diameter and volume and a significant decrease in LV fractional shortening and ejection fraction. Posterior wall thickening increased significantly, whereas septal thickening did not increase throughout DSE in both groups. CONCLUSIONS: In a subgroup of patients with HCM, DSE induces NWMA, associated with a greater increase in heart rate, irrespective of LVOTG. NWMA induce a depression of global LV systolic performance. The septum shows no contractile reserve, regardless of NWMA. These phenomena may be the result of induction of ischemia and/or impaired LV systolic function due to fast heart rate.

Myocardial collagen turnover in hypertrophic cardiomyopathy.

BACKGROUND: Myocardial interstitial fibrosis is a characteristic of hypertrophic cardiomyopathy (HCM). This study evaluates the collagen turnover in HCM and its impact on left ventricular (LV) diastolic function. METHODS AND RESULTS: Thirty-six HCM patients and 14 sex- and age-matched controls were studied. Collagen turnover was assessed as follows. By radioimmunoassay, a byproduct of collagen III synthesis (PIIINP) and 3 peptides resulting from collagen I synthesis (PICP and PINP) and degradation (ICTP) were measured. By ELISA, matrix metalloproteinases (MMPs) were determined, as follows: active MMP-2; active MMP-9; and MMP-1 as active, free (as active MMP-1 plus its precursor), and total (as free MMP-1 plus MMP-1/tissue inhibitor complexes). Tissue inhibitor of metalloproteinases-1 (TIMP-1) was also assayed. All patients underwent echocardiography. The difference in duration between transmitral forward (A) and pulmonary venous retrograde (AR) waves (A-Ar) was considered an estimate of passive diastolic function. Furthermore, restrictive or pseudonormal LV filling patterns were considered to identify patients with passive diastolic dysfunction. Patients had higher levels of PIIINP, ICTP, MMP-2, MMP-9, and total TIMP-1 than did controls. PIIINP was inversely related to LV end-diastolic diameter. A-Ar was inversely related to PICP, PINP, and their differences with ICTP (estimates of collagen I buildup). Furthermore, A-Ar was directly related to MMP-1 and MMP-2. CONCLUSIONS: As compared with controls, collagen turnover is enhanced in HCM patients. As collagen I synthesis prevails over degradation and MMP-1 and MMP-2 are inhibited, passive diastolic dysfunction occurs in patients with HCM.

Massive chronic atrial thrombosis.

We report herein a patient in whom a very large and old thrombus in the left atrium was detected by transesophageal echocardiography. The patient started warfarin and aspirin. After 2 years of therapy, transesophageal echocardiography showed the complete resolution of thrombus in the absence of clinical evidence of embolism. This case indicates that large and presumably organized thrombi may be dissolved by an anticoagulant therapy, although the lytic activity of warfarin has never been demonstrated. Transesophageal echocardiography helps in the identification and follow-up of such conditions and contributes to understanding of warfarin action in left atrial thrombosis.

Hemodynamic effects of isometric exercise in hypertrophic cardiomyopathy: comparison with normal subjects.

BACKGROUND: We assessed the hemodynamic effects of isometric exercise by an ambulatory radionuclide monitoring device (VEST) that measured left ventricular function in patients who had hypertrophic cardiomyopathy (HCM), with and without significant left ventricular outflow-tract obstruction at rest, compared with control subjects. METHODS AND RESULTS: We studied 10 patients with obstructive HCM, 25 patients with nonobstructive HCM, and 11 control subjects. During VEST monitoring, all patients gripped a dynamometer at 75% of maximal strength for up to 5 minutes. End-diastolic, end-systolic, and stroke volumes; cardiac output; and systemic vascular resistance were expressed as a percentage of baseline. The mean exercise duration was similar among the 3 groups. During handgrip, heart rate, systolic blood pressure, and cardiac output increased significantly and similarly in the 3 groups. There was a significant difference in the lung activity between obstructive and nonobstructive HCM patients and control subjects (P <.001), with a fall in control subjects and no change in HCM patients, irrespective of obstruction. Control subjects showed a decrease in end-systolic volume (P =.02) and an increase in ejection fraction (P =.003) and stroke volume (P =.009), whereas these parameters did not change in HCM patients, irrespective of obstruction. Systemic vascular resistance increased in obstructive (P =.02) and nonobstructive (P <.01) HCM patients but did not change in control subjects. CONCLUSIONS: Isometric exercise causes an abnormal and similar adaptation to load changes in obstructive and nonobstructive HCM patients, as compared with control subjects.