Left ventricular ejection fraction as therapeutic target: is it the ideal marker?

Heart failure (HF) consists the fastest growing clinical cardiac disease. HF patients are categorized on the basis of underlying left ventricular ejection fraction (LVEF) into HF with preserved EF (HFpEF), reduced LVEF (HFrEF), and mid-range LVEF (HFmrEF). While LVEF is the most commonly used surrogate marker of left ventricular (LV) systolic function, the implementation of two-dimensional echocardiography in estimating this parameter imposes certain caveats on current HF classification. Most importantly, LVEF could fluctuate in repeated measurements or even recover after treatment, thus blunting the borders between proposed categories of HF and enabling upward classification of patients. Under this prism, we sought to summarize possible procedures to improve systolic function in patients with HFrEF either naturally or by the means of pharmacologic and non-pharmacologic treatment and devices. Therefore, we reviewed established pharmacotherapy, including beta-blockers, inhibitors of renin-angiotensin-aldosterone axis, statins, and digoxin as well as novel treatments like sacubitril-valsartan, ranolazine, and ivabradine. In addition, we assessed evidence in favor of cardiac resynchronization therapy and exercise training programs. Finally, innovative therapeutic strategies, including stem cells, xanthine oxidase inhibitors, antibiotic regimens, and omega-3 polyunsaturated fatty acids, were also taken into consideration. We concluded that LVEF is subject to changes in HF after intervention and besides the aforementioned HFrEF, HFpEF, and HFmrEF categories, a new entity of HF patients with recovered LVEF should be acknowledged. An improved global and refined LV function assessment by sophisticated imaging modalities and circulating biomarkers is expected to render HF classification more accurate and indicate patients with viable-yet dysfunctional-myocardium and favorable characteristics as the ideal candidates for LVEF recovery by individualized HF therapy.

Pocket-sized point-of-care cardiac ultrasound devices : Role in the emergency department.

BACKGROUND: Acute breathlessness accounts for 8% of accident and emergency attendances. Point-of-care cardiac ultrasound (US) effectively reduces time to diagnosis. Fast and practical information via pocket-sized cardiac US devices may better the diagnosis in this complex patient group. METHODS: We prospectively enrolled 40 consecutive patients presenting with shortness of breath at the emergency department (ED). Divided into two groups were all adult patients over 18 with acute breathing difficulties (triage category 1-3): 21 patients received a short focused cardiac US scan using a pocket-sized Vscan and 19 patients received no scan. Data were obtained regarding the time taken for diagnosis and treatment, patient length of stay, inpatient mortality and 30-day mortality. RESULTS: In the scanned group 33% of patients had significantly abnormal Vscan results that had the potential to aid diagnosis and guide management. The difference of 20 min between the means of the time to diagnosis between the groups was not significant. DISCUSSION: The individual knowledge of UK emergency physicians regarding basic echocardiography varies greatly. An intuitive approach following a brief tutorial on pocket-size echocardiography was shown to improve diagnostic accuracy in addition to history taking and physical examination by medical students and junior doctors with no previous exposure to echocardiography. Increasing evidence shows the feasibility and benefit of FOCUS echo in the ED and the pocket-sized devices could play a large role. CONCLUSION: The Vscan is a practical, portable device that provides rapid diagnostic information. One third of patients had significant findings on the scans to possibly aid diagnosis and prevent misdiagnosis. This has the potential to reduce time to diagnosis in the ED.

Preeclampsia: What Does the Father Have to Do with It?

Preeclampsia (PE) is one of the leading causes of maternal and fetal morbidity and mortality, with incidence rates ranging between 2 and 5 % in the Western World. The exact causes of the disease remain largely unknown, because of the complex pathophysiologic mechanisms involved in the process. Genetic, environmental, and epigenetic parameters have been implicated by various authors as culprits for the pathogenesis of PE. Recent reports in the literature highlight the paternal role. Still, the exact extent and mechanism remain elusive. In this systematic review, we attempt to present data regarding the paternal role in a concise and comprehensive manner.

Aortic Stenosis, Aortic Regurgitation and Arterial Hypertension.

BACKGROUND: Hypertension (HT) is an important risk factor for cardiovascular disease and might precipitate pathology of the aortic valve. OBJECTIVE: To investigate the association of HT with aortic dysfunction (including both aortic regurgitation and stenosis) and the impact of antihypertensive treatment on the natural course of underlying aortic disease. METHODS: We performed a systematic review of the literature for all relevant articles assessing the correlation between HT and phenotype of aortic disease. RESULTS: Co-existence of HT with aortic stenosis and aortic regurgitation is highly prevalent in hypertensive patients and predicts a worse prognosis. Certain antihypertensive agents may improve haemodynamic parameters (aortic jet velocity, aortic regurgitation volume) and remodeling of the left ventricle, but there is no strong evidence of benefit regarding clinical outcomes. Renin-angiotensin system inhibitors, among other vasodilators, are well-tolerated in aortic stenosis. CONCLUSION: Several lines of evidence support a detrimental association between HT and aortic valve disease. Therefore, HT should be promptly treated in aortic valvulopathy. Despite conventional wisdom, specific vasodilators can be used with caution in aortic stenosis.

Differentiation between restrictive cardiomyopathy and constrictive pericarditis by early diastolic doppler myocardial velocity gradient at the posterior wall.

BACKGROUND: The differential diagnosis between restrictive cardiomyopathy (RCM) and constrictive pericarditis (CP) is challenging and, despite combined information from different diagnostic tests, surgical exploration is often necessary. METHODS AND RESULTS: A group of 55 subjects (mean age, 63+/-11 years; 36 men and 19 women) were enrolled in the study; 15 had RCM, 10 had CP, and 30 were age-matched, normal controls. The diagnosis of RCM was supported by a biopsy; in the CP group, the diagnosis was confirmed either surgically or at autopsy. All patients underwent a transthoracic echocardiogram that included the assessment of Doppler myocardial velocity gradient (MVG), as measured from the left ventricular posterior wall during the predetermined phases of the cardiac cycle. MVG was lower (P<0.01) in RCM patients compared with both CP patients and normal controls during ventricular ejection (2. 8+/-1.2 versus 4.4+/-1.0 and 4.7+/-0.8 s(-1), respectively) and rapid ventricular filling (1.9+/-0.8 versus 8.7+/-1.7 and 3.7+/-1.4 s(-1), respectively). Additionally, during isovolumic relaxation, MVG was positive in RCM patients and negative in both CP patients and normal controls (0.7+/-0.4 versus -1.0+/-0.6 and -0.4+/-0.3 s(-1), respectively; P<0.01). During atrial contraction, MVG was similarly low (P<0.01) in both RCM and CP patients compared with normal controls (1.6+/-1.7 and 1.7+/-1.8 versus 3.8+/-0.9 s(-1), respectively). CONCLUSIONS: Doppler myocardial imaging-derived MVG, as measured from the left ventricular posterior wall in early diastole during both isovolumic relaxation and rapid ventricular filling, allows for the discrimination of RCM from CP.

Increased proinflammatory cytokines in patients with chronic stable angina and their reduction by aspirin.

BACKGROUND: Proinflammatory cytokines released by injured endothelium facilitate interaction of endothelial cells with circulating leukocytes and thus may contribute to development and progression of atherosclerosis. We investigated whether cytokines and C-reactive protein (CRP) are indicative of myocardial ischemia or of diseased vessels and whether they are influenced by aspirin treatment in patients with chronic stable angina. METHODS AND RESULTS: Plasma macrophage colony stimulating factor (MCSF), IL-1b, IL-6, and CRP were measured in 60 stable patients after 48-hour Holter monitoring and in 24 matched controls. All patients had angiographic documentation of disease and positive exercise ECGs. Patients with ischemia on Holter monitoring (n=40) received aspirin or placebo in a 6-week, randomized, double blind, crossover trial. Blood sampling was repeated at the end of each treatment phase (3 weeks). Compared to controls, patients had more than twice median MCSF (800 versus 372 pg/mL), IL-6 (3.9 versus 1.7 pg/mL), and CRP (1.25 versus 0.23 mg/L) levels (P<0.01 for all comparisons). MCSF was related to ischemia on Holter monitoring (P<0.01), to low ischemic threshold during exercise (P<0.01), and together with IL-1b to number of diseased vessels (P<0.05). MCSF, IL-6, and CRP were all reduced after 6 weeks of aspirin treatment (P<0.05). CONCLUSIONS: These findings suggest that cytokines are associated with both ischemia and anatomic extent of disease in patients with stable angina. Reduced cytokine and CRP levels by aspirin may explain part of aspirin's therapeutic action.

Echocardiographic characterization of cardiomyopathy in Friedreich's ataxia with tissue Doppler echocardiographically derived myocardial velocity gradients.

BACKGROUND: Conventional and tissue Doppler echocardiographically derived myocardial velocity gradients (MVGs) were used to characterize the myocardium in patients with Friedreich's ataxia (FRDA), and the relationship between MVGs and the mutation in the FRDA gene, a GAA triplet repeat expansion, was investigated. METHODS AND RESULTS: We studied 29 patients with FRDA (10 men, mean age 31+/-9 years) who were homozygous for the GAA expansion in the FRDA gene and were without cardiac symptoms. A comparison was made with a group of 30 age-matched control subjects. In patients with FRDA, interventricular septal thickness (1.17+/-0.26 versus 0.85+/-0.13 cm, P:<0.005), posterior left ventricular wall thickness (1.00+/-0.24 versus 0.88+/-0.15 cm, P:<0.01), and left atrial diameter (3.3+/-0.5 versus 2.9+/-0.3 cm, P:=0.01) were increased compared with control subjects. MVGs were reduced in FRDA during systole (3.1+/-1.2 versus 4.5+/-0.5 s(-1), P:<0.0001) and in early diastole (4.9+/-2.7 versus 8.8+/-1.8 s(-1), P:<0.0001) but increased in late diastole (2.0+/-1. 3 versus 1.1+/-0.9 s(-1), P:<0.01). The strongest relationship was seen between age-corrected early diastolic MVGs and the GAA expansion in the smaller allele of the FRDA gene (r=-0.68, P:<0. 0001). CONCLUSIONS: MVGs offer a means of further characterizing the myocardial abnormalities in patients with FRDA. Early diastolic MVGs appear to relate most closely to the genetic abnormality and the consequential reduction in frataxin protein.

Significance of persistent left ventricular dysfunction during recovery after dobutamine stress echocardiography.

OBJECTIVES: This study sought to determine the duration of new or worsening left ventricular regional wall motion abnormalities (RWMAs) after dobutamine stress echocardiography (DSE) and their relation to the extent of coronary artery disease (CAD). BACKGROUND: Despite extensive reports on DSE, little is known about the duration of new or worsening RWMAs during recovery. We hypothesized that the persistence of RWMAs during recovery may be associated with the extent of CAD and therefore ischemia. METHODS: Sixty-five consecutive patients with positive results on DSE and angiographically documented CAD were studied. Each patient underwent 12-lead electrocardiography and two-dimensional echocardiography at rest, during dobutamine infusion and continuously during recovery to assess the recovery time of ischemic myocardial regions. RESULTS: All patients had at least one ischemic region during DSE. Complete resolution of RWMAs occurred within 25 min in patients with multivessel CAD, within 20 min in those with two-vessel disease and within 15 min in those with single-vessel disease (p < 0.001). The greater the wall motion score index at peak stress, the longer the duration of RWMAs into the recovery phase (p < 0.01). RWMAs persisted long after normalization of each patient's symptoms, electrocardiographic (ECG) changes, heart rate and rate-pressure product during recovery. CONCLUSIONS: We demonstrated that normalization of left ventricular RWMAs occurs after resolution of symptoms and ECG changes during recovery. The time to recovery is related to the extent of CAD and myocardial ischemia as well as to the presence or absence of collateral circulation. These findings may represent stunned myocardium after brief period of ischemia.

Comparison of dobutamine and treadmill exercise echocardiography in inducing ischemia in patients with coronary artery disease.

OBJECTIVES: We sought to compare the magnitude of ischemia precipitated by both treadmill exercise and dobutamine stress echocardiography. BACKGROUND: Although it is alleged that dobutamine stress produces ischemia similar in degree and extent to that produced during treadmill exercise, a direct comparison with treadmill exercise, the most common form of exercise, has not been performed. METHODS: Eighty-five consecutive patients with known coronary artery disease underwent both stress tests on the same day, in random order. RESULTS: Sixty-two patients (73%) had positive results on exercise echocardiography compared with 53 (62%) who had positive results on dobutamine stress (p = NS). Of the 53 patients with positive dobutamine test results, wall motion abnormalities appeared after the addition of atropine in 35 patients (66%). During dobutamine infusion, 22 patients (26%) had a hypotensive response that was reversed in 16 by prompt administration of atropine. At peak dobutamine-atropine stress, heart rate was higher than that at peak exercise (p < 0.001), whereas systolic blood pressure and rate-pressure product were higher at peak exercise than at peak dobutamine-atropine stress (p = 0.0001). In the 53 patients with positive results on both tests, peak wall motion score index was greater with treadmill exercise than with dobutamine-atropine infusion ([mean +/- SD] 1.73 +/- 0.45 vs. 1.57 +/- 0.44, p < 0.001). CONCLUSIONS: Echocardiography immediately after treadmill exercise induces a greater ischemic burden than dobutamine-atropine infusion. In the clinical setting, exercise echocardiography should therefore be chosen over dobutamine echocardiography for diagnosing ischemia, when possible. When dobutamine echocardiography is used as an alternative modality, maximal heart rate should always be achieved by the addition of atropine.

Clinical evaluation of left heart Doppler contrast enhancement by a saccharide-based transpulmonary contrast agent. The Levovist Cardiac Working Group.

OBJECTIVES: A multicenter study was carried out to evaluate the efficacy with which SHU 508A enhances left heart Doppler signals and improves the clinical quantification of valve disease. BACKGROUND: Poor signal-to-noise ratio often limits the Doppler interrogation of left heart flows. This problem may be resolved by the enhancement of Doppler signals by an ultrasound contrast agent capable of pulmonary transmission, such as the recently developed SHU 508A. METHODS: Left heart contrast enhancement was tested for 1) continuous wave Doppler evaluation in 51 patients with aortic stenosis, 2) pulsed Doppler transthoracic evaluation of pulmonary venous flow in 85 patients, and 3) color Doppler evaluation of mitral regurgitation in 60 patients. Studies were performed immediately before and during the intravenous administration of SHU 508A (16 ml of 200 mg/ml) and compared with unenhanced transesophageal data in representative subsets of patients. RESULTS: SHU 508A had no serious adverse effects. A significant increase in left heart Doppler signal intensity lasted for 30 to 300 s. The continuous wave Doppler velocity envelope was enhanced for all jets, but Doppler peak velocity was not altered in high quality baseline studies. However, Doppler contrast enhancement resulted in higher measured peak gradients (p < 0.001) in 29 patients with aortic stenosis who had poor quality baseline studies. This improved the overall correlation with invasive pressure measurements (r = 0.73 vs. r = 0.89, p < 0.01). The enhanced pulsed Doppler traces of transthoracic pulmonary venous flow allowed quantitative analysis in 92% patients (vs. 27% at baseline) and correlated well with peak velocities and velocity profiles obtained by transesophageal echocardiography (r = 0.91, p < 0.001). The enhanced color Doppler display of regurgitant jets increased jet area with a high interindividual variability (mean 276%), resulting in almost identical jet areas as unenhanced transesophageal values (r = 0.97, p < 0.001). CONCLUSIONS: SHU 508A is a safe transpulmonary contrast agent that significantly enhances both spectral and color Doppler signals in the left heart. In specific patient subsets, the increase in signal-to-noise ratio improved the quantitative assessment of aortic stenosis, pulmonary venous flow and mitral regurgitation.

Magnitude of myocardial dysfunction is greater in painful than in painless myocardial ischemia: an exercise echocardiographic study.

OBJECTIVES: This study sought to assess the presence and extent of inducible myocardial dysfunction during painful and painless (silent) myocardial ischemia in a homogeneous patient cohort with coronary artery disease and no previous myocardial infarction. BACKGROUND: The functional significance of painless versus painful demand-driven ischemia remains controversial, with conflicting results in published reports regarding the amount of myocardium in jeopardy. METHODS: Exercise echocardiography was performed in 89 patients (mean [+/- SD] age 59.3 +/- 8.2 years) with significant coronary artery disease and positive exercise stress test results. Patients were taking no antianginal medications and were classified into painless and painful cohorts after the outcome of a symptom-limited treadmill exercise test. No patients had previous coronary artery bypass surgery. Images were acquired in digital format before and immediately after treadmill exercise testing. RESULTS: Fifty-eight patients had painful and 31 painless myocardial ischemia. Clinical and demographic characteristics as well as coronary artery anatomy were similar in both groups. Patients with painless ischemia achieved better exercise performance with greater exercise duration (p < 0.001) and higher maximal rate-blood pressure product (p < 0.001) than those with painful ischemia. New wall motion abnormalities were seen in 54 patients (93%) with painful versus 17 (55%) with painless ischemia (p < 0.001). Total ischemic score was greater in patients with painful than in those with painless ischemia (15.9 +/- 3.7 vs. 12 +/- 1.4, p < 0.001, respectively), with a greater number of ischemic myocardial segments in painful than in painless ischemia (101 [16%] vs. 21 [6%], p < 0.001, respectively). CONCLUSIONS: Patients with painless ischemia frequently have regional myocardial dysfunction on exertion detected by echocardiography, but painful episodes are accompanied by a greater magnitude of myocardial dysfunction.

Absence of myocardial dysfunction during stress in patients with syndrome X.

Stress two-dimensional echocardiographic studies were performed in 18 patients with angina, a positive exercise test and normal findings on coronary angiography (syndrome X). Rest and immediate posttreadmill exercise two-dimensional echocardiograms were performed with a digitized cine loop and side by side visual analysis in all patients. In 16 of these patients, right atrial pacing up to 160 beats/min was also performed and percent systolic wall thickening was calculated at five equally spaced segments around the left ventricle, each corresponding to an anterior, lateral and inferior wall and the posterior and the anterior ventricular septum. Measurements of percent systolic wall thickening were established in 10 age- and gender-matched normal persons for comparison. ST segment depression occurred in all patients during exercise and persisted for 42.1 s (range 18 to 75) into the recovery period. Immediate postexercise echocardiography was started within 20.1 +/- 5.4 s and completed in 54.1 +/- 11.3 s. No patient had regional wall motion abnormalities seen on two-dimensional imaging of any myocardial segment. Thirteen patients (72%) reported reproduction of their usual chest pain, which led to termination of the test. During rapid right atrial pacing, nine patients (56%) developed ST segment depression that was associated with angina in seven. In all 16 patients, percent systolic wall thickening increased over values at rest in each myocardial segment. Percent systolic wall thickening averaged 47.1 +/- 6.1% at rest and increased to 74 +/- 8% during right atrial pacing (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Accuracy of two-dimensional echocardiography in the diagnosis of aortic arch obstruction.

To evaluate the predictive accuracy of two-dimensional echocardiography in the diagnosis of aortic arch obstruction, 540 consecutive patients aged 2 days to 15 years (mean 2 months) who underwent subsequent cardiac catheterization and angiography were prospectively studied. At angiography, 51 patients had aortic arch obstruction; of these, 35 had juxtaductal coarctation, 15 isthmic hypoplasia and 1 a type B interrupted aortic arch. The presence of arch obstruction was correctly identified with two-dimensional echocardiography in 45 of 51 patients with this condition (overall sensitivity 88%). Two-dimensional echocardiography clearly defined a juxtaductal coarctation in 33 of 35 patients and isthmic hypoplasia in 13 of 15 patients (sensitivity 94% and 73%, respectively). The form and type of interrupted aortic arch were clearly distinguished from other forms and types of arch obstruction. Among the 489 patients without aortic arch obstruction, two-dimensional echocardiography wrongly diagnosed the presence of such obstruction in 9 patients (overall specificity 98%). Forty-six (92%) of the 51 patients had at least one associated intracardiac abnormality. Twenty-two (44%) had a ventricular septal defect, 21 (42%) a bicuspid aortic valve and 4 (18%) subaortic stenosis. Five patients had complex congenital cardiac malformations. All associated abnormalities were prospectively identified with two-dimensional echocardiography. Thus, two-dimensional echocardiography is highly specific in diagnosing aortic arch obstruction. It is less sensitive for the diagnosis of isthmic hypoplasia in the neonatal period.

Echocardiographic assessment of the right ventricle in Ebstein's anomaly: relation to clinical outcome.

Two-dimensional echocardiography was performed in 16 patients with Ebstein's anomaly to assess right ventricular anatomy and function in relation to clinical features and prognosis. Measurements of right ventricular anatomy and function were established in 10 normal subjects for comparison. Ten patients were in New York Heart Association functional class I, four in class II and one each in classes III and IV. Right ventricular morphology and the three tricuspid valve leaflets were assessed from right ventricular inflow tract and apical four chamber views. The anterior tricuspid leaflet was abnormal but not displaced in all patients; the septal and posterior leaflets were displaced in 14 (88%) and 11 (69%) patients respectively. The posterior leaflet was best visualized from the right ventricular inflow tract, and in two patients this view was required for the echocardiographic diagnosis of Ebstein's anomaly, based on displacement of the septal tricuspid valve leaflet. An index of right ventricular function, the fractional area contraction, was defined as the difference between the end-diastolic and the end-systolic area, normalized to the end-diastolic area. This index was calculated for both the proximal (atrialized) right ventricle and the total right ventricle. Total right ventricular end-diastolic area and fractional area contraction exceeded 95% confidence limits when compared with values in the normal group. During a median follow-up period of 4 years three patients died. They had severe right heart morphologic or functional abnormalities; two were in functional class III or IV and one was asymptomatic. None of the survivors had severe symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

Diastolic function in hypertrophic cardiomyopathy: relation to exercise capacity.

Doppler echocardiography was used to assess diastolic function in 40 patients with hypertrophic cardiomyopathy and to relate it to the patients' symptoms, anaerobic threshold and maximal oxygen consumption during cardiopulmonary exercise testing. The patients had a smaller early (E wave) (p less than 0.01), higher late (A wave) (p less than 0.05) mitral diastolic flow velocity, larger A/E ratio (p less than 0.01), longer isovolumetric relaxation time and E wave duration (p less than 0.001) and slower deceleration rate of the E wave (p less than 0.001) than 40 age- and gender-matched normal subjects. In the patients with hypertrophic cardiomyopathy, maximal oxygen consumption and anaerobic threshold were, respectively, 26.3 +/- 9.2 and 21.1 +/- 6.1 ml/kg per min compared with 47 (range 39 to 68) (p less than 0.01) and 41 (range 27 to 58) ml/kg per min (p less than 0.01) in normal subjects. There was no relation between Doppler indexes and symptoms but symptomatic patients had lower maximal oxygen consumption and anaerobic threshold compared with asymptomatic patients (21.4 +/- 7 vs. 30.7 +/- 10, p less than 0.001 and 18.6 +/- 4.7 vs. 23.1 +/- 5.7, respectively, p less than 0.001). In conclusion, Doppler echocardiography can identify abnormalities of left ventricular filling in patients with hypertrophic cardiomyopathy. However, these indexes measured at rest do not correspond to the patient's professed symptomatic status or exercise capacity measured objectively. Conversely, cardiopulmonary exercise testing reveals a depressed maximal oxygen consumption and anaerobic threshold even in the least symptomatic patients.

Echocardiographic measurement of right ventricular wall thickness in hypertrophic cardiomyopathy: relation to clinical and prognostic features.

Hypertrophic cardiomyopathy is characterized by unexplained left ventricular hypertrophy. It is uncertain, however, to what extent the right ventricle is also thickened. Right ventricular hypertrophy is found at autopsy in patients who die suddenly but, until recently, systematic evaluation of right ventricular morphology has not been feasible. In this two-dimensional echocardiographic study, a total of 4 to 10 (median 7) right ventricular wall thickness measurements were made from six right ventricular views in 73 patients with hypertrophic cardiomyopathy. Forty-one normal subjects were also studied for comparison. Thirty-two (44%) of the 73 patients had right ventricular hypertrophy with at least two of the wall thickness measurements exceeding 2 standard deviations (SD) from the mean value in the normal subjects. Right ventricular hypertrophy was mild (less than or equal to 8 mm) in 24 patients, moderate (9 to 12 mm) in 7 and severe (greater than 12 mm) in 1. The coefficient of variation of right ventricular wall thickness measurements was similar in normal subjects and patients with and without right ventricular hypertrophy (17 +/- 7, 11 +/- 8 and 10 +/- 8, respectively). The hypertrophy was concentric, with a coefficient of variation of 25% in all but one patient. There was a strong correlation of maximal right and mean left ventricular wall thickness (r = 0.643, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiographic measures of left ventricular structure and their relation with rest and ambulatory blood pressure in blacks and whites in the United Kingdom.

OBJECTIVES: This study attempted to determine whether people of black African descent have more left ventricular hypertrophy than those of white European descent and whether this can be explained by rest or ambulatory blood pressure. BACKGROUND: Mortality associated with hypertension is higher in black populations than among whites, but differences in morbidity and their associations with blood pressure are inconsistent. METHODS: We examined 1,166 black and white men and women 40 to 64 years old in a community survey in London, United Kingdom. Echocardiograms were obtained for all subjects and ambulatory blood pressure recordings for 319. RESULTS: Adjusted for body size, ventricular septal thickness was greater in blacks than whites (p < 0.05), and cavity dimension was smaller (p < 0.05). In men, ventricular septal thickness was > 10 mm for 32% of whites and 53% of blacks; for women these figures were 14% and 38%, respectively. Relative wall thickness was greater in blacks (p < 0.01 for men and women), but left ventricular mass index was similar in the two ethnic groups. In men, hypertension resulted in an increase in wall thickness in both ethnic groups, but cavity dimension decreased in blacks and increased in whites. Wall thickness was higher in blacks than in whites for equivalent levels of either rest (p = 0.05) or ambulatory (p = 0.007) blood pressure. CONCLUSIONS: Left ventricular mass index may not be valid for comparison between ethnic groups because this derived measure does not take into account ethnic differences in ventricular structural response to hypertension. Interventricular wall thickness may be more valid. Using this measure, we demonstrate greater ventricular hypertrophy in blacks than in whites, unexplained by differences in either rest or ambulatory blood pressure. The pattern of ventricular hypertrophy observed in blacks is associated with an increased mortality risk. Conventional blood pressure thresholds for instituting antihypertensive treatment may be too conservative for people of black African descent.

The natural history of left ventricular thrombus in myocardial infarction: a rationale in support of masterly inactivity.

One hundred five unselected and consecutive patients were prospectively studies after acute transmural myocardial infarction to assess the incidence of mural thrombus formation and to relate the presence of thrombus to patient outcome in terms of systemic embolic events, functional class and survival. In 87 patients, optimal quality two-dimensional echocardiographic studies were obtained and were repeated at daily intervals to detect mural thrombus formation. The site of infarction was anterior in 53 patients and inferior in 34. On admission, all patients received subcutaneous heparin and antiplatelet agents (aspirin, dipyridamole); none received full anticoagulant therapy. Left ventricular mural thrombus was visualized between 2 and 11 days (median 6) after the clinical onset of infarction in 21 (40%) of the 53 patients with anterior infarction. No patients with inferior infarction had echocardiographic evidence of thrombus formation. During follow-up of 22 to 51 months (mean 39), none of the 21 patients with mural thrombus had clinical evidence of systemic embolism. One patient with inferior and one with anterior infarction had a cerebral embolus 7 days and 9 months, respectively, after the acute event, but neither of these patients had echocardiographic evidence of left ventricular thrombus at any stage. Echocardiography performed at 1 and 2 years of follow-up showed persistent evidence of thrombus in only 8 (31%) and 5 (24%) of the 21 patients, respectively. On admission, the functional class of patients with anterior myocardial infarction and thrombus was similar to that of patients without ventricular thrombus.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac syndrome X: clinical characteristics and left ventricular function. Long-term follow-up study.

OBJECTIVES: Our aim was to study the clinical characteristics and evolution of symptoms and left ventricular function in a clinically homogeneous group of patients with syndrome X (angina pectoris, positive exercise test results and normal coronary arteriograms). BACKGROUND: The syndrome of angina with normal coronary arteriograms is heterogeneous and encompasses different pathogenetic entities. These characteristics may contribute to the existing controversy concerning the cause of syndrome X. METHODS: We studied 99 patients with syndrome X (78 women, 21 men; mean age +/- SD 48.5 +/- 8 years). All underwent clinical characterization, ambulatory electrocardiographic (ECG) monitoring and echocardiographic assessment of left ventricular function during a follow-up period of 7 +/- 4 years. RESULTS: The syndrome was more common in women than in men. Of the women, 61.5% were postmenopausal before the onset of chest pain. All 99 patients had exertional angina, and 41 also had rest angina. The average duration of episodes of chest pain was > 10 min in 53% of patients. Sublingual nitrate was effective for relief of pain in 42% of patients. Transient ST segment depression was observed during ambulatory ECG monitoring in 64 patients and myocardial perfusion abnormalities in 22. During the first stage of the exercise test, 32 patients had an increase > 20 mm Hg in systolic blood pressure and showed an earlier onset of ST depression and shorter exercise time than did patients whose blood pressure increased < or = 20%. During follow-up, no deaths or myocardial infarctions occurred, ventricular function was unchanged (shortening fraction 35.4 +/- 4% vs. 35.6 +/- 3%; heart failure developed in only one patient), systemic hypertension occurred in eight patients and conduction disturbances in four. Symptoms lessened in 11 patients, were variable or unchanged in 64 and worsened in 24. CONCLUSIONS: Syndrome X, as defined in this study, occurs predominantly in postmenopausal women. Patients usually have chest pain typical for angina, but conventional antianginal treatment is not often successful. Myocardial perfusion abnormalities occur in a small proportion of patients. Long-term survival is not adversely affected, and deterioration of cardiac function rarely occurs.

Arrhythmia and prognosis in infants, children and adolescents with hypertrophic cardiomyopathy.

In adults with hypertrophic cardiomyopathy, the annual mortality rate from sudden death is 2 to 3%, and the finding of nonsustained ventricular tachycardia during electrocardiographic (ECG) monitoring provides a marker of the patient who is at increased risk. In the young, the annual mortality rate from sudden death is even higher, approximately 6%, but the prognostic significance of arrhythmia is unknown. To determine the prevalence of arrhythmia and its relation to prognosis, 2 days of ECG monitoring was performed in 6 infants, 14 children and 33 adolescents with hypertrophic cardiomyopathy receiving no cardioactive medications. An additional 1 to 9 days (median 2) of monitoring was performed in 29 patients. All patients had sinus rhythm; 4 adolescents had episodes of paroxysmal supraventricular tachycardia, a child with the Wolff-Parkinson-White syndrome had symptomatic reentrant atrioventricular tachycardia and 5 adolescents had asymptomatic nonsustained ventricular tachycardia. During follow-up of 1 week to 7 years (median 3 years), five patients died suddenly and two had successful resuscitation from out-of-hospital ventricular fibrillation; none of these seven patients had ventricular arrhythmias during 2 to 7 days (median 3) of ECG monitoring. The two patients with ventricular fibrillation, the five with ventricular tachycardia, the one with Wolff-Parkinson-White syndrome and the seven with recurrent syncope or adverse family history, or both, received low dose amiodarone. None of these "high risk" patients died during 6 months to 6 years (median 3 years) of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)