_________________________T ricuspid and pulmonary valve regurgitation usually occurs as a secondary phenomenon caused by dilatation of the valve ring secondary to right ventricular failure or pulmonary hypertension, respectively. Primary diseases of the tricuspid or pulmonary valves are uncommon, but the more likely causes might include congenital abnormalities, rheumatic heart disease, or infective endocarditis. Carcinoid heart disease is a rare, but interesting and important cause of intrinsic tricuspid and pulmonary valve disease leading to significant morbidity and mortality caused by right heart failure. When treated medically, and in appropriate cases surgically, significant benefits in overall quality of life and long term survival can be achieved. We review the current literature regarding the pathophysiological basis of the disease, the cardiovascular complications, and the currently available treatment strategies. AETIOLOGY AND PATHOPHYSIOLOGYc Carcinoid tumours are rare neuroendocrine malignancies arising from neural crest amine precursor uptake decarboxylation cells. Approximately 90% of all carcinoid tumours are located in the gastrointestinal system of which the most common sites are the appendix and terminal ileum. Other less common sites include the bronchus and gonads. The most malignant of the carcinoid tumours tend to arise from the ileum and must be invasive or metastasise to produce the carcinoid syndrome which is characterised by facial flushing, intractable secretory diarrhoea, and bronchoconstriction. The incidence of carcinoid tumours is approximately 1 in 75 000 of the population 1 of whom about 50% develop carcinoid syndrome. Once the carcinoid syndrome has developed, approximately 50% of these patients develop carcinoid heart disease which typically causes abnormalities of the right side of the heart. Usually, only carcinoid tumours that invade the liver result in pathological changes to the heart. The cardiac manifestations are caused by the paraneoplastic effects of vasoactive substances such as 5-hydroxytryptamine (5-HT or serotonin), histamine, tachykinins, and prostaglandins released by the malignant cells rather than any direct metastatic involvement of the heart. Ordinarily, the vasoactive tumour products are inactivated by the liver, lungs, and brain, but the presence of hepatic metastases may allow large quantities of these substances to reach the right side of the heart without being inactivated by the liver.The characteristic pathological findings are endocardial plaques of fibrous tissue that may involve the tricuspid valve, pulmonary valve, cardiac chambers, venae cavae, pulmonary artery, and coronary sinus. The fibrous reaction may involve not only the valve leaflets, but also the subvalvar apparatus including the tendinous chords and papillary muscles of the tricuspid valve, and more rarely the mitral valve in cases with left sided involvement. The fibrous tissue in the plaques results in distortion of the valves leading to either stenosis, regurgitation, or both. The p...

Independent of the severity of coronary artery disease, diabetic patients have an increased risk of developing heart failure. This clinical entity has been considered to be a distinct disease process referred to as 'diabetic cardiomyopathy'. Experimental studies suggest that extensive metabolic perturbations may underlie both functional and structural alterations of the diabetic myocardium. Translational studies are, however, limited and only partly explain why diabetic patients are at increased risk of cardiomyopathy and heart failure. Although a range of diagnostic methods may help to characterize alterations in cardiac function in general, none are specific for the alterations in diabetes. Treatment paradigms are very much limited to interpretation and translation from the results of interventions in non-diabetic patients with heart failure. This suggests that there is an urgent need to conduct pathogenetic, diagnostic and therapeutic studies specifically in diabetic patients with cardiomyopathy to better understand the factors which initiate and progress diabetic cardiomyopathy and to develop more effective treatments.

Background-The aim of this study was to compare the risk conferred by white-coat versus sustained mild hypertension for the development of cardiovascular disease. Methods and Results-Patients (nϭ479) who underwent 24-hour intra-arterial ambulatory blood pressure monitoring on the basis of a persistently elevated clinic systolic blood pressure of 140 to 180 mm Hg were followed up for the development of subsequent cardiovascular events during a 9.1Ϯ4.2-year period. White-coat hypertension, defined as a clinic systolic blood pressure of 140 to 180 mm Hg associated with a 24-hour ambulatory systolic blood pressure Ͻ140 mm Hg and diastolic blood pressure Ͻ90 mm Hg, was present in 126 patients, and the remainder had sustained mild hypertension. A subgroup of patients without complications underwent follow-up echocardiography and carotid ultrasound. White-coat hypertensives were younger (44Ϯ12 versus 52Ϯ10 years, respectively; PϽ0.001) and had a significantly lower incidence of cardiovascular events (1.32 versus 2.56 events per 100 patient-years, respectively; PϽ0.001) than sustained hypertensives. Multivariate analysis revealed age (Pϭ0.002), sex (Pϭ0.007), race (Pϭ0.001), smoking (Pϭ0.005), and the presence of white-coat hypertension (hazard ratio, 0.29; 95% CI, 0.09 to 0.90; Pϭ0.04) to be independent predictors of subsequent cardiovascular events. Subgroup analysis in patients without complications revealed a lower incidence of left ventricular hypertrophy and lesser degrees of carotid hypertrophy in the white-coat group. Conclusions-These findings indicate a relatively benign outcome in white-coat hypertension compared with sustained mild hypertension. (Circulation. 1998;98:1892-1897.)

Background-This study compared the relative prognostic significance of 24 hour intra-arterial ambulatory systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and pulse pressure (PP) parameters in middle-aged versus elderly hypertensives. Methods and Results-A total of 546 subjects aged Ͻ60 years and 142 subjects aged Ն60 years who had undergone baseline pretreatment 24-hour intra-arterial ambulatory blood pressure monitoring were followed for 9.2Ϯ4.1 years. Multivariate analysis showed that in younger subjects, 24-hour, daytime, and nighttime DBP, MAP, and SBP, when considered individually, were positively related to morbid events; DBP parameters provided the best predictive values.In the group Ն60 years (elderly group), 24-hour, daytime, and nighttime PP and SBP were the most predictive parameters, whereas ambulatory DBP and MAP measurements failed to provide any prognostic value. When 24-hour values of SBP and DBP were jointly included in the baseline model, DBP (zϭ2.02, Pϭ0.04) but not SBP (zϭϪ0.43, Pϭ0.67) was related to outcome in younger subjects, whereas in the elderly group, SBP (zϭ3.33, Pϭ0.001) was positively and DBP (zϭϪ1.75, Pϭ0.07) was negatively related to outcome. Clinic blood pressure measurements failed to provide any independent prognostic value in either age group. Conclusions-The relative prognostic significance of ambulatory blood pressure components depends on age; DBP parameters provided the best prognostic value in middle-aged individuals, whereas PP parameters were the most predictive in the elderly. This may reflect differing underlying hemodynamic mechanisms of hypertension in these age groups.

Through the establishment of a cardio-oncology service, it is feasible to achieve high rates of cardiac optimisation and cancer treatment continuation.

This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Pulmonary arterial dissection is an extremely rare and usually lethal complication of chronic pulmonary hypertension. The condition usually manifests as cardiogenic shock or sudden death and is therefore typically diagnosed at postmortem examination rather than during life. However, recent isolated reports have described pulmonary artery dissection in surviving patients. The first case of pulmonary artery dissection in a surviving patient with cor pulmonale caused by chronic obstructive pulmonary disease is presented. The aetiology, pathophysiology, and clinical presentation of pulmonary artery dissection are reviewed and factors that may aid diagnosis during life are discussed.A lthough dissection of the systemic arteries is a well recognised and often non-fatal consequence of essential hypertension, pulmonary arterial dissection is an extremely rare and usually lethal complication of chronic pulmonary hypertension. Pulmonary artery dissection has most commonly been described in patients with underlying congenital heart disease and in those with primary pulmonary hypertension. The condition usually manifests as cardiogenic shock or sudden death and is therefore typically diagnosed at postmortem examination rather than during life. [1][2][3][4] However, recent isolated reports have described pulmonary artery dissection in surviving patients. Despite the relatively common causal association of chronic obstructive pulmonary disease with pulmonary hypertension, pulmonary artery dissection has rarely been reported in this group of patients. We present the first case of pulmonary artery dissection in a surviving patient with cor pulmonale caused by chronic obstructive pulmonary disease. We also review the aetiology, pathophysiology, and clinical presentation of pulmonary artery dissection and discuss factors that may aid diagnosis during life. CASE REPORTA 56 year old woman presented to the emergency department with notable shortness of breath and mild bilateral leg oedema. About 30 years previously, she had had extensive pulmonary tuberculosis treated with streptomycin. Since then she had experienced mild dyspnoea on exertion but over the preceding six months her exercise capacity had reduced greatly to about 50 m. Three weeks before admission, she had developed a productive cough and malaise. She had also noticed an isolated episode of a severe, sharp pain in the upper back radiating to the left anterior chest and arms associated with sweating and lasting for about 10 minutes. At that time she was empirically treated with antibiotics resulting in resolution of the cough, but the dyspnoea continued to worsen and was accompanied by the development of peripheral oedema. She was a longstanding heavy smoker; she did not have any pets, and there was no history of occupational dust exposure. Clinical examination showed a thin body habitus, respiratory rate of 22 breaths/min, resting tremor, peripheral cyanosis, palmar erythema, and mild kyphoscoliosis. She was afebrile, her heart rate was 100 beats/min, and her blood pres...

A very large body of evidence--predominantly retrospective--suggests that revascularization is superior to optimal medical therapy in patients with a significant amount of 'hibernating' myocardium. Contemporary cardiological practice has embraced this standard of practice, as many centres worldwide place great emphasis upon the results of viability testing by non-invasive imaging techniques in determining the need for coronary revascularization. This practice has been challenged by the recent results of the Surgical Treatment for Ischaemic Heart Failure (STICH) trial, which suggested both lack of mortality benefit from revascularization and also from viability testing. In this review article, we have summarized the pathophysiology of hibernating myocardium, briefly discussed each of the non-invasive imaging modalities used in contemporary practice for detecting myocardial hibernation before critically appraising the prospective studies in this field, most importantly the main STICH trial and viability sub-study. STICH was clearly a complex trial but has not ended the question over the benefit of revascularization in ischaemic heart failure. Finally, we have suggested a possible methodology for an 'ideal trial' designed to evaluate the role of revascularization in such patients and also explored how viability testing should be used in clinical practice in the post-STICH era.