Preheart failure comorbidities and impact on prognosis in heart failure patients: a nationwide study.

BACKGROUND: Data regarding the impact of preheart failure (HF) comorbidities on the prognosis of HF are scarce, especially in the younger HF patients. OBJECTIVES: To investigate pre-existing comorbidities in HF patients versus matched controls and to assess their impact on mortality. METHODS: We included all first-time in-hospital and outpatient diagnoses of HF from 1995 to 2017, and comorbidities antedating the HF-diagnosis in the Danish nationwide registries. HF patients were matched with up to five controls. One-year all-cause mortality rates and population attributable risk (PAR) were estimated for three separate age groups (≤50, 51-74 and >74 years). RESULTS: Totally 280 002 patients with HF and 1 166 773 controls were included. Cardiovascular comorbidities, for example, cerebrovascular disease and ischaemic heart disease were more frequent in the oldest (17.9% and 29.7% in HF vs. 9.8% and 10.7% in controls) compared to the youngest age group (3.9% and 15.2% in HF vs. 0.7% and 0.9% in controls). Amongst patients with HF, 1-year mortality rates (per 100 person-years) were highest amongst those with >1 noncardiovascular comorbidity: ≤50 years (10.4; 9.64-11.3), 51-74 years (23.3; 22.9-23.7), >74 years (58.5; 57.9-59.0); hazard ratios 245.18 (141.45-424.76), 45.85 (42.77-49.15) and 24.5 (23.64-25.68) for those ≤50, 51-74 and >74 years, respectively. For HF patients ≤50 years, PAR was greatest for hypertension (17.8%), cancer (14.1%) and alcohol abuse (8.5%). For those aged >74 years, PAR was greatest for hypertension (23.6%), cerebrovascular disease (6.2%) and cancer (7.2%). CONCLUSIONS: Heart failure patients had a higher burden of pre-existing comorbidities, compared to controls, which adversely impacted prognosis, especially in the young.

Genome-wide meta-analysis of variant-by-diuretic interactions as modulators of lipid traits in persons of European and African ancestry.

Hypertension (HTN) is a significant risk factor for cardiovascular morbidity and mortality. Metabolic abnormalities, including adverse cholesterol and triglycerides (TG) profiles, are frequent comorbid findings with HTN and contribute to cardiovascular disease. Diuretics, which are used to treat HTN and heart failure, have been associated with worsening of fasting lipid concentrations. Genome-wide meta-analyses with 39,710 European-ancestry (EA) individuals and 9925 African-ancestry (AA) individuals were performed to identify genetic variants that modify the effect of loop or thiazide diuretic use on blood lipid concentrations. Both longitudinal and cross sectional data were used to compute cohort-specific interaction results, which were then combined through meta-analysis in each ancestry. These ancestry-specific results were further combined through trans-ancestry meta-analysis. Analysis of EA data identified two genome-wide significant (p < 5 × 10-8) loci with single nucleotide variant (SNV)-loop diuretic interaction on TG concentrations (including COL11A1). Analysis of AA data identified one genome-wide significant locus adjacent to BMP2 with SNV-loop diuretic interaction on TG concentrations. Trans-ancestry analysis strengthened evidence of association for SNV-loop diuretic interaction at two loci (KIAA1217 and BAALC). There were few significant SNV-thiazide diuretic interaction associations on TG concentrations and for either diuretic on cholesterol concentrations. Several promising loci were identified that may implicate biologic pathways that contribute to adverse metabolic side effects from diuretic therapy.

Predicting decline of kidney function in lupus nephritis using urine biomarkers.

OBJECTIVE: To evaluate candidate biomarkers to predict future renal function decline (RFD) in children and adults with lupus nephritis (LN). METHODS: At the time of enrollment into prospective observational LN cohort studies liver-type fatty acid binding protein (LFABP), albumin, monocyte chemoattractant protein-1 (MCP-1), uromodulin, transferrin, and hepcidin were measured in urine samples of two cohorts of patients with LN, one followed at a pediatric (cohort-1; n = 28) and one at an adult institution (cohort-2; n = 69). The primary outcome was RFD, defined in cohort-1 as a decrease in estimated glomerular filtration rate (eGFR) of ≥20% and in cohort-2 as a sustained increase of ≥25% in serum creatinine concentration (SCr), both from baseline. RESULTS: All patients (n = 97) had normal eGFR or SCr at the time of urine collection at baseline. RFD occurred in 29% (8/28) of patients in cohort-1 during a mean follow-up of 6.1 months, and in 30% (21/69) of those in cohort-2 during a mean follow-up of 60 months. Individually, in cohort-1, levels of MCP-1, transferrin, LFABP, and albumin were higher in the RFD group than those who maintained renal function, with statistical significance for LFABP and albumin. In cohort-2 the RFD group also had higher levels of urine MCP-1 and albumin than others. The combination of LFABP, MCP-1, albumin, and transferrin had good predictive accuracy for RFD in both cohorts (area under the ROC curve = 0.77-0.82). CONCLUSION: The combinatorial urine biomarker LFABP, MCP-1, albumin, and transferrin shows promise as a predictor of renal functional decline in LN, and warrants further investigation.

Clinical correlates of sex steroids and gonadotropins in men over the late adulthood: the Framingham Heart Study.

Low serum concentrations of sex steroids and gonadotropins in men have been associated with increased cardiometabolic risk and mortality, but the clinical correlates of these hormones in men over late adulthood are less clearly understood. We analysed up to five serial measurements of total testosterone (TT), dehydroepiandrosterone sulphate (DHEAS), follicle stimulating hormone (FSH), luteinizing hormone (LH) and total estradiol (EST) in older men in the original cohort of the Framingham Heart Study to determine the short- (2-years; 1,165 person-observations in 528 individuals) and long-term (up to 10-years follow-up; 2520 person-observations in 835 individuals with mean baseline age: 71.2 years) clinical correlates of these sex steroids and gonadotropins using multilevel modelling and Generalized Estimating Equations. Age, body mass index and pre-existing type 2 diabetes were inversely related to long-term TT concentrations, whereas higher systolic blood pressure showed a positive association. Furthermore, age and pre-existing cardiovascular disease (CVD) were inversely associated and HDL cholesterol concentrations positively associated with long-term DHEAS concentrations respectively. Analyses of short-term changes revealed age was inversely related to DHEAS, but positively related to FSH and LH concentrations. Our community-based study identified modifiable correlates of decreasing TT and DHEAS concentrations in elderly men, suggesting that maintenance of a low CVD risk factor burden may mitigate the age-related decline of these hormones over the late adulthood.

Endogenous circulating testosterone and sex hormone-binding globulin levels and measures of myocardial structure and function: the Framingham Heart Study.

BACKGROUND: The relation between endogenous testosterone concentrations and myocardial mass and function remains incompletely understood. OBJECTIVES: To determine the cross-sectional association between endogenous hormone levels with cardiac magnetic resonance measures of myocardial mass, structure, and function in community-dwelling men across a wide age range. METHODS: A total of 720 men from the Framingham Heart Study Offspring Cohort (age range 37-82, mean = 59.6 years) who underwent cardiac magnetic resonance imaging and had hormone levels measured. Total testosterone (measured using liquid chromatography-tandem mass spectrometry), sex hormone-binding globulin (measured using an immunofluorometric assay), and calculated free testosterone levels were assessed in male participants of the Framingham Heart Study Offspring Cohort at examination 7. Cardiac magnetic resonance imaging was performed between examinations 7 and 8 (2002-2006). RESULTS: Age-adjusted linear regression models showed statistically significant association between total testosterone levels and left ventricular mass (p = 0.009), left ventricular mass index (p = 0.006), cardiac output (p = 0.001), and main pulmonary artery diameter (p = 0.008); the association between total testosterone and these cardiac magnetic resonance measures was weak and was not significant after adjustment for established risk factors-age, body mass index, diabetes, and hypertension. Furthermore, calculated free testosterone level was not significantly associated with any measure of myocardial mass or function. Sex hormone-binding globulin level was significantly associated with left ventricular mass (p = 0.002), left ventricular mass index (p = 0.004), cardiac output (p = 0.003), left ventricular ejection fraction (p = 0.039), and main pulmonary artery diameter (p = 0.042) in age-adjusted models; these associations were also rendered non-significant after adjusting for cardiovascular risk factors. CONCLUSIONS: Neither testosterone nor sex hormone-binding globulin levels in men are associated significantly with myocardial mass and function independent of established cardiovascular risk factors.

Clinical and genetic correlates of soluble P-selectin in the community.

BACKGROUND: P-selectin is a cell adhesion molecule that is involved in atherogenesis, and soluble concentrations of this biomarker reflect cardiovascular risk. However, the clinical correlates and genetic characterization of soluble P-selectin have not been clearly elucidated. OBJECTIVE: To describe clinical and genetic correlates of circulating P-selectin in the community. METHODS: In Framingham Heart Study Offspring (European descent) and Omni (ethnic/racial minority) participants, we examined the association of cardiovascular risk factors with soluble P-selectin concentrations. In Offspring participants, we evaluated heritability, linkage and association of 29 SELP single-nucleotide polymorphisms (SNPs) with adjusted P-selectin concentrations. RESULTS: In multivariable analysis of 3,690 participants (54% women, mean age 60 +/- 10 years), higher log-transformed P-selectin concentrations were inversely associated with female sex and hormone replacement therapy, and positively associated with age, ethnic/racial minority status, cigarette smoking, waist circumference, systolic blood pressure, fasting glucose, and total/high-density lipoprotein cholesterol and triglyceride concentrations. Clinical factors explained 10.4% of the interindividual variability in P-selectin concentrations. In 571 extended pedigrees (n = 1,841) with >or= 2 phenotyped members per family, multivariable-adjusted heritability was 45.4 +/- 5.8%. Among the SELP SNPs examined, a non-synonymous SNP (rs6136) encoding a threonine-to-proline substitution at position 715 was highly significantly associated with decreased P-selectin concentrations (P = 5.2 x 10(-39)), explaining 9.7% of variation after adjustment for clinical factors. CONCLUSIONS: Multiple clinical factors and an SNP in the SELP gene were significantly associated with circulating P-selectin concentrations. One SNP in SELP explained significant variation in circulating P-selectin concentrations, even after accounting for known clinical correlates.

Risk factors for acute ischaemic stroke in young adults in South India.

BACKGROUND: Stroke is a leading cause of death and disability in developing countries, afflicting individuals at a young age. The contribution of established vascular risk factors to ischaemic stroke in young adults has not been evaluated systematically in Indians. METHODS: We conducted a case control study in 214 South Indian patients with first acute ischaemic stroke that occurred between the ages of 15 and 45 years, 99 age and sex matched hospital controls and 96 community controls. We compared the prevalence of the following risk factors: smoking, elevated blood pressure, high fasting blood glucose and abnormal lipids. RESULTS: Compared with community controls, stroke patients had a higher prevalence of smoking (multivariable adjusted odds ratio (OR) 7.77, 95% CI 1.93 to 31.27), higher systolic blood pressure (OR per SD increment of 1.88, 95% CI 1.01 to 3.49) and fasting blood glucose (OR per SD increment of 4.55, 95% CI 1.63 to 12.67), but lower high density lipoprotein (HDL) cholesterol (OR per SD increment of 0.17, 95% CI 0.09 to 0.30). Compared with hospital controls, stroke patients had a higher prevalence of smoking (OR 3.95, 95% CI 1.61 to 9.71) and lower HDL cholesterol (OR per SD increment 0.27, 95% CI 0.17 to 0.44). The presence of > or = 3 metabolic syndrome components was associated strongly with stroke (OR 4.76, 95% CI 1.93 to 11.76; OR 2.09, 95% CI 1.06 to 4.13) compared with community and hospital controls. CONCLUSIONS: Key components of the metabolic syndrome and smoking are associated with ischaemic stroke in young South Indian adults. Our observations underscore the importance of targeting adolescents and young adults for screening and prevention to reduce the burden of ischaemic stroke in young adults.

Associations of objective physical activity with insulin sensitivity and circulating adipokine profile: the Framingham Heart Study.

The purpose of this study was to explore the relation of physical activity (PA) and sedentary time (SED) to insulin sensitivity and adipokines. We assessed PA and SED using Actical accelerometers and insulin resistance (HOMA-IR) in 2109 participants (free of type 1 and 2 diabetes mellitus) from Framingham Generation 3 and Omni 2 cohorts (mean age 46 years, 54% women). Systemic inflammation (C-reactive protein [CRP]) and circulating adipokines were measured 6 years earlier. Steps per day, moderate-to-vigorous PA (MVPA) and SED per wear time (%SED) were predictor variables in multivariable regression analyses, with HOMA-IR, CRP and circulating adipokines as outcome measures. We reported that higher MVPA and more steps per day were associated with lower HOMA-IR, adjusting for %SED (ß = -0.036, P = 0.002; ß = -0.041, P = 0.005). Steps were inversely associated with CRP, but were directly associated with insulin-like growth factor (IGF)-1 levels (ß = -0.111, P = 0.002; ß = 3.293, P = 0.007). %SED was positively associated with HOMA-IR (ß = 0.033, P < 0.0001), but non-significant after adjusting for MVPA (P = 0.13). %SED was associated with higher ratio of leptin/leptin receptor (sOB-R) and higher adipocyte fatty acid-binding protein (FABP)4 (ß = 0.096, P < 0.0001; ß = 0.593, P = 0.002). Our findings suggest differential influences of PA vs. SED on metabolic pathways, with PA modulating insulin resistance and inflammation, whereas SED influences FABPs.

Plasminogen activator inhibitor and the risk of cardiovascular disease: The Framingham Heart Study.

INTRODUCTION: Although plasminogen activator inhibitor (PAI-1) plays a key regulatory role in fibrinolysis, it has not been clearly shown to independently predict cardiovascular disease (CVD) among individuals without prior CVD. We investigated, in the Framingham Heart Study offspring cohort, whether PAI-1 predicted CVD risk among individuals without prior CVD. METHODS: Plasma PAI-1 antigen and tissue plasminogen activator (TPA) antigen were measured in 3203 subjects without prior CVD between 1991 and 1995; average follow-up of 10 years. PAI-1 was remeasured 4 years after baseline, to determine the effect of serial change on risk. RESULTS: PAI-1 levels (mean ± SD) were 29.1 ng/ml (19.2) versus 22.1 (16.5) for those and without incident CVD; p<0.001, and TPA levels were 12.0 ng/ml (5.7) versus 9.0 (4.7); p<0.001. PAI-1 and TPA antigen levels had a strong unadjusted linear relation with incident CVD (p<0.001). After adjustment for conventional risk factors, the hazard ratios (HRs) for higher quartiles of PAI-1, compared with the lowest, were 1.9, 1.9, 2.6 (linear trend p=0.006), and 1.6, 1.6, 2.9 (p<0.001) for TPA antigen. The adjusted HRs for increasing quartiles of serial change in PAI-1 at 4 years, compared with the lowest, were 0.9, 0.8, 1.3 (p=0.050). C statistic assessment showed that adding PAI-1 or TPA to conventional risk factors resulted in small increases in discrimination and modest reclassification of risk, which was statistically significant for TPA (net reclassification 6.8%, p=0.037) but not PAI-1 (4.8%, p=0.113). CONCLUSION: PAI-1 and TPA antigen levels are predictive of CVD events after accounting for established risk factors. A serial increase in PAI-1 is associated with a further increase in risk. These findings support the importance of fibrinolytic potential in CVD.

Prevalence, clinical features and prognosis of diastolic heart failure: an epidemiologic perspective.

Numerous reports suggest that about one-third of patients with congestive heart failure do not have any abnormality of left ventricular systolic function. These patients presumably have heart failure on the basis of ventricular diastolic dysfunction. Our objective was to develop a comprehensive overview of published reports of the prevalence, clinical features and prognosis of diastolic heart failure and to offer recommendations for future studies. Thirty-one studies of patients with congestive heart failure with normal left ventricular systolic function were published in the time period from January 1970 through March 1995. These studies were identified with the use of computer-based searches in relevant data bases. Among patients with congestive heart failure, the prevalence of normal ventricular systolic performance in the published reports varies widely from 13% to 74%; the reported annual mortality rate also varies from 1.3% to 17.5%. The criteria for congestive heart failure, its chronicity and the age of the study sample affect the reported prevalence and prognosis of the disorder. The clinical signs and symptoms of diastolic heart failure are similar to those of patients with systolic heart failure, underscoring the need for evaluation of ventricular systolic function in patients with congestive heart failure. In the absence of any large-scale randomized clinical trial targeting these patients, the optimal treatment of diastolic heart failure is unclear. We conclude that the heterogeneity in previous studies of diastolic heart failure hinders the comparison of published reports. There is a need to conduct prospective, community-based investigations to better characterize the incidence, prevalence and natural history of diastolic heart failure. Randomized clinical trials are needed to determine optimal treatment strategies.

Value and limitations of Doppler echocardiographic determination of mitral valve area in Lutembacher syndrome.

OBJECTIVES: Our objective was to compare the Doppler pressure half-time, Doppler continuity equation and two-dimensional echocardiographic planimetric methods of estimating mitral valve area in Lutembacher syndrome. BACKGROUND: Fluid dynamics theory predicts that mitral pressure half-time varies inversely with mitral valve area and directly with net chamber compliance and the peak early diastolic transmitral gradient in pure mitral stenosis. The effects of an atrial shunt on these interrelations have not been investigated. METHODS: Correlation and agreement between mitral valve area estimates obtained by the three methods and that obtained by cardiac catheterization was ascertained in 11 patients with Lutembacher syndrome. RESULTS: Valve areas determined by planimetry and the continuity equation method correlated and agreed well with catheterization measurements (r = 0.83 and 0.81, respectively). The pressure half-time method consistently overestimated mitral valve area; the extent of overestimation was greater in patients with larger atrial shunts. The hemodynamic pressure half-time was independent of the mitral valve area, chamber compliance and the peak transmitral gradient. It was dependent on the magnitude of the atrial shunt, although the correlation obtained was only fair (r = 0.61). CONCLUSIONS: These findings suggest that the Doppler pressure half-time method is an inaccurate measure of mitral valve area whenever an atrial shunt coexists with mitral stenosis. Planimetry and the Doppler continuity equation methods yield accurate estimates of mitral valve area in Lutembacher syndrome.

Congestive heart failure in subjects with normal versus reduced left ventricular ejection fraction: prevalence and mortality in a population-based cohort.

OBJECTIVES: The purpose of this study was to assess the relative proportions of normal versus impaired left ventricular (LV) systolic function among persons with congestive heart failure (CHF) in the community and to compare their long-term mortality during follow-up. BACKGROUND: Several hospital-based investigations have reported that a high proportion of subjects with CHF have normal LV systolic function. The prevalence and prognosis of CHF with normal LV systolic function in the community are not known. METHODS: We evaluated the echocardiograms of 73 Framingham Heart Study subjects with CHF (33 women, 40 men, mean age 73 years) and 146 age- and gender-matched control subjects (nested case-control study). Impaired LV systolic function was defined as an LV ejection fraction (LVEF) <0.50. RESULTS: Thirty-seven CHF cases (51%) had a normal LVEF; 36 (49%) had a reduced LVEF. Women predominated in the former group (65%), whereas men constituted 75% of the latter group. During a median follow-up of 6.2 years, CHF cases with normal LVEF experienced an annual mortality of 8.7% versus 3.0% for matched control subjects (adjusted hazards ratio = 4.06, 95% confidence interval 1.61 to 10.26). Congestive heart failure cases with reduced LVEF had an annual mortality of 18.9% versus 4.1% for matched control subjects (adjusted hazards ratio = 4.31, 95% confidence interval 1.98 to 9.36). CONCLUSIONS: Normal LV systolic function is often found in persons with CHF in the community and is more common in women than in men. Although CHF cases with normal LVEF have a lower mortality risk than cases with reduced LVEF, they have a fourfold mortality risk compared with control subjects who are free of CHF.

The role of hypertension in the pathogenesis of heart failure. A clinical mechanistic overview.

Hypertension plays a key role in the evolution of the syndrome of heart failure. Hypertension has been identified as the chief precursor of left ventricular hypertrophy. Hypertensive left ventricular hypertrophy can lead to ventricular diastolic dysfunction; it is also a risk factor for myocardial infarction, which is a principal cause of left ventricular systolic dysfunction. Asymptomatic left ventricular dysfunction, whether systolic or diastolic, culminates in clinically overt heart failure when a threshold is exceeded or when other precipitating factors are superimposed. The onset of overt heart failure heralds a bleak outcome. These structural and functional changes associated with hypertension evolve over decades and are preventable with effective antihypertensive treatment. These observations emphasize the importance of early diagnosis and effective treatment of hypertension to prevent cardiac complications.

Congestive heart failure with normal left ventricular systolic function. Clinical approaches to the diagnosis and treatment of diastolic heart failure.

The syndrome of congestive heart failure with preserved left ventricular systolic function is common in clinical practice. The signs and symptoms of the disorder are similar to those of congestive heart failure with left ventricular systolic dysfunction, underscoring a need for routine evaluation of left and right ventricular systolic function in patients with congestive heart failure. The syndrome may be related to anatomic abnormalities that increase the resistance to ventricular filling, or to physiologic abnormalities of myocardial relaxation or compliance. Advancing age, often in association with hypertension, coronary artery disease, tachycardia, and atrial fibrillation, is commonly associated with the disorder. Randomized controlled clinical trials are needed to evaluate the efficacy of various therapeutic agents in reducing the risks associated with diastolic heart failure.

Elevated midlife blood pressure increases stroke risk in elderly persons: the Framingham Study.

BACKGROUND: Stroke risk predictions are traditionally based on current blood pressure (BP). The potential impact of a subject's past BP experience (antecedent BP) is unknown. We assessed the incremental impact of antecedent BP on the risk of ischemic stroke. METHODS: A total of 5197 stroke-free subjects (2330 men) in the community-based Framingham Study cohort were enrolled from September 29, 1948, to April 25, 1953, and followed up to December 31, 1998. We determined the 10-year risk of completed initial ischemic stroke for 60-, 70-, and 80-year-old subjects as a function of their current BP (at baseline), recent antecedent BP (average of readings at biennial examinations 1-9 years before baseline), and remote antecedent BP (average at biennial examinations 10-19 years earlier), with adjustment for smoking and diabetes mellitus. Models incorporating antecedent BP were also adjusted for baseline BP. The effect of each BP component (systolic BP, diastolic BP, and pulse pressure) was assessed separately. RESULTS: Four hundred ninety-one ischemic strokes (209 in men) were observed in eligible subjects. The antecedent BP influenced the 10-year stroke risk at the age of 60 years (relative risk per SD increment of recent antecedent systolic BP: women, 1.68 [95% confidence interval, 1.25-2.25]; and men, 1.92 [95% confidence interval, 1.39-2.66]) and at the age of 70 years (relative risk per SD increment of recent antecedent systolic BP: women, 1.66 [95% confidence interval, 1.28-2.14]; and men, 1.30 [95% confidence interval, 0.97-1.75]). This effect was evident for recent and remote antecedent BP, consistent in hypertensive and nonhypertensive subjects, and demonstrable for all BP components. CONCLUSIONS: Antecedent BP contributes to the future risk of ischemic stroke. Optimal prevention of late-life stroke will likely require control of midlife BP.

Usefulness of antimyosin antibody imaging for the detection of active rheumatic myocarditis.

Myocarditis constitutes an important component of rheumatic carditis. Antimyosin scintigraphy, which allows noninvasive assessment of myocyte damage, can be used for documentation of cardiac involvement in patients with rheumatic fever where clinical diagnosis is not unequivocal.

Echocardiographic reference values for aortic root size: the Framingham Heart Study.

The objectives of this study were to develop sex-, age-, and body size-specific nomograms and partition values for upper and lower limits of M-mode echocardiographic aortic root measurements derived from a large population-based cohort. The study sample consisted of 1433 male and 1816 female participants in the Framingham Heart Study and Framingham Offspring Study who were normotensive and free of clinically apparent heart disease at the baseline examination. Aortic root measurements were obtained by M-mode echocardiography by a leading-edge to leading-edge technique. The relations of age and measures of body size with aortic root dimensions were evaluated with sex-specific correlations and multiple stepwise linear regression analyses. Age was the most important determinant of aortic root size in both men and women in the multivariable regression models. Models with age and body surface area yielded R2 values of 0.214 in men and 0.222 in women. Models with age and height yielded lower R2 values of 0.136 in men and 0.181 in women. Thus aortic root dimensions vary widely with the age, sex, and body size of individuals. Sex-specific reference nomograms of aortic root dimensions in relation to age and body size (body surface area or height) are presented to facilitate the detection of abnormalities of aortic root size.

Trigeminal and peripheral neuropathy in a patient with systemic sclerosis and silicosis.

The unusual occurrence of cranial (trigeminal) and peripheral neuropathy in a case of progressive systemic sclerosis (PSS) is described. The possible association of PSS with silicosis is also discussed.

Unusual electrocardiographic response during pulmonary balloon valvoplasty.

An 18-year-old girl with severe valvar pulmonary stenosis was subjected to balloon valvoplasty. During each inflation of the balloon, we observed transient electrocardiographic disappearance of 'R' waves in the monitoring lead. The possible explanations for this observation include sudden severe right ventricular strain and ischemia.

Myocardial infarction associated with a myocardial bridge.

A 30-year-old man was admitted with severe chest pain and electrocardiographic evidence of myocardial infarction. Subsequent angiography revealed myocardial bridging of the middle third of the left anterior descending coronary artery and no evidence of coronary atherosclerosis. In the absence of other risk factors, circumstantial evidence points to a possible etiological role of myocardial bridging in the ischemic event in our patient.