Clinical applications of coronary sinus retroperfusion during high risk percutaneous transluminal coronary angioplasty.

OBJECTIVES: This study was designed to determine the efficacy of synchronized coronary sinus retroperfusion of arterial blood in reducing myocardial ischemia associated with the performance of high risk coronary angioplasty. BACKGROUND: Previous animal and clinical work has demonstrated the efficacy of this technique in supporting ischemic myocardium. METHODS: Twenty-one patients were randomized to alternately receive coronary sinus retroperfusion support during either the second or the third coronary angioplasty balloon inflation, after an initial unsupported brief control inflation. Myocardial ischemia was assessed by the extent of echocardiographic left ventricular wall motion abnormality, quantified ST segment deviation and hemodynamic and anginal variables during balloon inflations performed with and without coronary sinus retroperfusion support. Regional wall motion score was defined as hyperkinesia (-1), normokinesia (0), hypokinesia (+1), akinesia (+2) and dyskinesia (+3). RESULTS: A reduction in the echocardiographic left anterior descending regional wall motion score in retroperfusion-supported (1.7 +/- 2.1) versus unsupported (2.7 +/- 1.6) inflations (p < 0.05) was noted. Twelve-lead electrocardiographic monitoring revealed no additional ST segment deviation during supported (173 +/- 95 s) compared with unsupported (129 +/- 87 s) angioplasty inflations despite a significantly longer duration of supported inflations (p < 0.004). Mean and peak systolic coronary sinus pressures differed during supported inflations (21 +/- 6 and 44 +/- 13 mm Hg) versus unsupported inflations (10 +/- 4 and 16 +/- 5 mm Hg) (p < 0.001). There was no difference in hemodynamic or anginal variables. CONCLUSIONS: A reduction in ischemia as defined by wall motion abnormality during retroperfusion-supported compared with unsupported angioplasty balloon inflations was documented. No additional ST segment deviation occurred during retroperfusion-supported compared with unsupported balloon inflations despite a significantly longer duration of supported inflations. No difference in hemodynamic or anginal variables was noted.

Diagnosis of aortic pseudoaneurysm by echocardiography.

The diagnosis of pseudoaneurysm of the ascending aorta is of paramount importance because of its propensity to rupture. As the frequency of surgical procedures involving the aortic root and valve increases, an increase in the incidence of aortic pseudoaneurysm may be anticipated. We recently studied a patient who developed pseudoaneurysm of the ascending aorta following repair of a Type I aortic dissection, utilizing a composite graft. Two-dimensional echocardiography with color flow and pulsed Doppler imaging showed a large perigraft cavity communicating with the aorta. Echocardiography provides a safe noninvasive diagnostic tool for the evaluation of the aorta postoperatively and for screening for pseudoaneurysm formation in the follow-up period.

Diagnosis of recurrent left ventricular pseudoaneurysm by echocardiography with color flow imaging.

Left ventricular pseudoaneurysms are a rare complication of myocardial rupture. The diagnosis is paramount because of the propensity of pseudoaneurysms to rupture. Color flow imaging has been reported to be an aid in the diagnosis of pseudoaneurysms. We recently studied a patient with a myocardial infarction who developed a left ventricular pseudoaneurysm. Diagnosis was made by two-dimensional imaging with color flow imaging. He subsequently had a repair procedure with a gortex graft. One week after repair, repeat echocardiography with color flow imaging showed flow into the aneurysmal sac at multiple sites, consistent with recurrence of the pseudoaneurysm. Echocardiography with color flow imaging provides a safe noninvasive diagnostic tool for evaluating pseudoaneurysms preoperatively and in assessing the competency of the repair postoperatively.

Left ventricular filling in hypertensive blacks and whites following adrenergic blockade.

Left ventricular diastolic filling was investigated in 12 black and 15 white subjects before and after double-blinded randomized treatment of mild to moderate hypertension with combined alpha- and beta-adrenergic receptor blockade (labetalol) and beta-blockade alone (atenolol). At baseline (off medication), both groups were similar for age (46 +/- 8 years v 48 +/- 12 years), mean blood pressure (121 +/- 8 mm Hg v 115 +/- 8 mm Hg), left ventricular dimensions, left ventricular mass index (118 +/- 24 g/m2 v 113 +/- 13 g/m2), and left ventricular filling as reflected by transmitral flow velocity ratio A/E (0.97 +/- 0.33 v 0.92 +/- 0.19, normal age-matched control A/E ratio is 0.64 +/- 14). There were 6 blacks and 6 whites in the labetalol group; 6 blacks and 9 whites in the atenolol group. At six weeks of treatment, whites in the labetalol group showed a significantly greater drop in mean blood pressure (114 +/- 7/102 +/- 11, P less than .007 v 123 +/- 9/114 +/- 11, P = NS) and correspondingly greater improvement in A/E ratio (1.04 +/- 0.14/0.74 +/- 0.23, P less than .024 v 1.02 +/- 0.23/0.89 +/- 0.16, P = NS). However, this difference was no longer significant when controlling for age and blood pressure level. In the atenolol group, whites showed a significant increase in the rapid filling phase velocity E, while late filling phase velocity A significantly dropped only in blacks, without significant improvement in A/E ratio in either subgroup. In conclusion, greater improvement in left ventricular filling is seen with combined alpha-beta-blockade than beta-blockade alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of age on left ventricular filling in children of hypertensive parents.

Doppler transmitral flow velocity A/E ratio is a useful noninvasive estimate of left ventricular (LV) filling. However, the A/E ratio increases with age. To evaluate the effect of age on LV filling in children, Doppler transmitral flow velocity A/E ratios and echocardiographic measurements were obtained in 51 normal children (mean age 12 +/- 4 years) of hypertensive parents (study children), sex- and age-matched against 28 normal children (mean age 12 +/- 4 years) from normotensive parents (control children). There was a significant correlation between age and LV systolic and diastolic internal dimensions (r = 0.74 and 0.83, respectively, P less than .0001, in study children, and r = 0.70 and 0.79, respectively, P less than .0001, in control children), total wall thickness (r = 0.72, P less than .0001, in study children, and 0.61, P less than .001, in control children), and with LV mass index (r = 0.56, P less than .0001 and r = 0.45, P less than .02, respectively). In contrast, there was no correlation between age and transmitral flow velocity A/E ratio in either group (r = 0.12 and 0.07, respectively). In conclusion, age does not have an effect on LV filling in normal children from either normotensive or hypertensive parents. Therefore, age correction of A/E ration, which is necessary in adults, is not required in children. Because of a strong correlation between age and LV mass as well as LV mass index, age should be taken into account when defining criteria for LV hypertrophy in children.

Left ventricular function in mild hypertension after adrenergic blockade.

We previously used the Doppler transmitral flow velocity ratio A/E (A = late ventricular filling peak velocity; E = early ventricular filling peak velocity) and the age-adjusted ratio A/E/Age to detect left ventricular filling abnormalities in untreated mild hypertension. This study is a double-blind assessment of the effect of combined alpha- and beta-blockade (labetalol) and beta-blockade alone (atenolol) on left ventricular filling in mild hypertension. Twenty-seven patients blindly randomized to labetalol (12 patients) and atenolol (15 patients) treatment completed the echocardiographic and Doppler studies. Clinical and echo-Doppler data obtained at baseline and 6 weeks after initiation of therapy showed no difference between the two groups for age (49 +/- 10 vs 46 +/- 10 years), mean blood pressure (before therapy, 118 +/- 9 vs 117 +/- 8 mm Hg; after therapy, 108 +/- 12 mm Hg), left ventricular dimensions, wall thickness, systolic function, and mean late filling velocity A. There was no significant change in left ventricular mass and mass index with labetalol (left ventricular mass, 211 +/- 36 vs 216 +/- 38; mass index, 110 +/- 17 vs 112 +/- 16) or atenolol (245 +/- 41 vs 271 +/- 65; 120 +/- 18 vs 130 +/- 35). The mean velocity E, A/E, and A/E/Age ratios significantly improved with labetalol (p less than 0.05) but did not change significantly with atenolol. The improvement in A/E and A/E/Age ratios was primarily due to an increase in early filling velocity E.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac performance in children with homozygous sickle cell disease.

Cardiac function was evaluated in 24 children from a Jamaican sickle cell cohort study. Ten patients with sickle cell disease underwent echocardiographic studies on their eighth birthday. The results were compared with 14 age- and sex-matched control children born within hours of the index patients. Left ventricular dimension index (systolic 2.89 +/- 0.31 versus 2.33 +/- 0.42 cm and diastolic 4.70 +/- 0.35 versus 3.64 +/- 0.48 cm, p = 0.001), diastolic volume (79.4 +/- 17.1 versus 60.8 +/- 7.8 ml, p = 0.01), left ventricular mass index (116.3 +/- 3.4 versus 74.3 +/- 15.2 g/m2, p = 0.001) and cardiac index (5.51 +/- 1.32 versus 3.38 +/- 0.85 liters/min per m2 p = 0.001) were significantly increased in patients with sickle cell disease compared with values in control subjects. However, there was no statistically significant difference between the two groups for ejection fraction, velocity of circumferential fiber shortening, percent fractional shortening, systolic time intervals, wall stress and ratio of wall stress-systolic volume. Although two mean ratios of wall stress-systolic volume index were lower in children with sickle cell disease as compared with control subjects (4.0 +/- 0.7 versus 5.4 +/- 1.7, p = 0.02 and 5.9 +/- 1.2 versus 8.3 +/- 2.5, p = 0.005, respectively), the range of ratios remained within normal limits (3.4 to 5.8 in children with sickle cell disease versus 2.8 to 9.5 in controls and 4.2 to 8.3 versus 3.8 to 12.5, respectively). Furthermore, only body surface area predicted group status independent of other variables (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Right ventricular inflow and outflow obstruction due to adrenal cell carcinoma.

A 48-year-old man with surgically removed adrenal cell carcinoma presented with shortness of breath and fatigue. Physical examination revealed neck vein distention and a new systolic murmur. Echocardiography showed a right ventricular mass causing inflow and outflow tract obstruction. These findings were confirmed at surgery.

Diagnosis of pseudoaneurysm of the ascending aorta by pulsed Doppler cross sectional echocardiography.

Pseudoaneurysms of the ascending aorta are relatively uncommon compared with those evolving from the left ventricle. In a young man with endocarditis of the aortic valve who developed a pseudoaneurysm arising from the ascending aorta, the diagnosis was established with the pulsed Doppler technique and cross sectional echocardiography by passing the Doppler sample from the aorta through the neck of the false aneurysm into the large pseudoaneurysm. Aortic root angiography showed this connexion to be a small fistula between the aorta and right atrium. Necropsy findings confirmed the diagnosis.

Intermittent premature mitral valve closure in combined acute severe aortic and mitral regurgitation.

We have described the clinical, hemodynamic, and echocardiographic features of torn aortic cusps with mitral valve fenestration in a patient with infective endocarditis. Hemodynamic studies showed left atrial pressure intermittently exceeding left ventricular end-diastolic pressure. This phenomenon corresponded with intermittent premature mitral valve closure, which may serve as a marker for M-mode echocardiographic diagnosis in combined severe acute aortic and mitral regurgitation.

Systolic flutter of the tricuspid valve associated with massive pulmonary embolism.

We describe a patient with massive pulmonary embolism and resultant acute cor pulmonale and severe tricuspid incompetence. Fine systolic tricuspid valve flutter was detected by echocardiography during the acute phase, but the flutter disappeared as the patient improved clinically and the signs of tricuspid incompetence were no longer observed. Systolic flutter of tricuspid valve may serve as a useful clue in treating patients with severe tricuspid incompetence due to acute cor pulmonale.

Myocardial infarction and coronary ectasia in idiopathipc mitral valve prolapse syndrome.

Angina pectoris and myocardial infarction occurred in two patients with idiopathic mitral valve prolapse in the absence of atherosclerotic coronary artery disease. Instead, both patients showed the presence of coronary artery ectasia on cineangiography. The anatomic localization of ectasia corresponded with segmental derangement of left ventricular wall motion. Repeated thromboemboli from ectatic vessels and/or locally liberated platelet metabolites were considered the probable mechanism of these symptoms.

On the role of tortuous coronary arteries in billowing mitral leaflet syndrome. A hypothesis.

Sixty three male patients with billowing mitral leaflet syndrome (BML) and forty one age and sex match controls were studied with emphasis on the cineangiographic features of coronary arteries. In the BML group, the coronary arteries were considered normal in five and abnormal in fifty eight. In fifty eight with abnormal coronary arteries, twelve showed atherosclerotic occlusive lesions, fifteen showed combined occlusive lesions and nonocclusive abnormalities and thirty one showed nonocclusive abnormalities alone. The non-atherosclerotic abnormalities consisted of redundancy of the coronary arteries manifested by bizarre changes in configuration and motion. These abnormalities were present in only five patients in the Control Group. On the basis of our observations and corroborative evdience in the literature, a hypothesis is presented; the salient features of which are that: (1) the spectrum of BML may be considerably more complex than hitherto suspected, (2) a combination of BML and tortuous coronary arteries may form a distinct subset of this spectrum and (3) the increased tortuousity may result in impaired coronary perfusion causing myocardial ischemia thus offering a possible explanation for some of the symptoms - such as chest pain, arrhythmias and even sudden death seen in this syndrome.