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PubMed1991

Unique cardioprotective potential of angiotensin converting enzyme inhibitors: a hypothesis still to be tested on humans.

'Primary cardioprotection' has, arguably, already been shown with thiazide diuretics and probably with beta-blockers. The proven safety and efficacy of these established drugs override any theoretical or experimental considerations in favour of ACE inhibitors. It is unfortunate that, as yet, the number of hypotheses generated in support of ACE inhibitors has not been matched by large scale clinical trials employing these drugs. The first report of the clinical use of an ACE inhibitor was in 1984; it is high time comparative studies with conventional, and proven, agents were undertaken. With regard to 'secondary cardioprotection', there is overwhelming evidence in favour of the use of beta-blockers in patients with myocardial ischaemia. Indeed, we would argue that ACE inhibitors should be used with caution in such patients to avoid impairment of coronary infusion. In the patient with acute myocardial infarction, intravenous nitrates are cheap, easy to use, safe and seem to be effective (in preventing early remodelling and reducing mortality). In the subacute phase, beta-blockers improve prognosis and, according to the currently available evidence in humans, nitrates are as effective as captopril in altering late remodelling; as in the acute situation, nitrates are cheaper, simpler to use and have a track record of long-term safety. ACE inhibitors improve symptoms, exercise capacity and prognosis in chronic heart failure. In this condition, they have been a major therapeutic advance and, on the available evidence, are to be initially preferred to other vasodilators though they should be given in addition to diuretics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1997

Regulation of contractile proteins in diabetic heart.

Diabetes is one of the most prevalent chronic conditions that has a high association with death from cardiovascular disease(s). An impaired cardiac function independent of vascular disease suggests the existence of a primary myocardial defect in diabetes mellitus. We and others have documented that myocardial performance is impaired in the hearts of chronically diabetic rats and rabbits. Abnormalities in the contractile proteins and regulatory proteins could be responsible for the mechanical defects in streptozotocin (STZ)-diabetic hearts. The major focus of research on contractile proteins in the diabetic state has been on myosin ATPase and its isoenzymes. However, in the contractile protein system, this could be only one of the mechanisms that might be a controlling factor in myofilament contraction in diabetes. To define the role of cardiac contractile as well as regulatory proteins (troponin-tropomyosin) as a whole in the regulation of actomyosin system in diabetic cardiomyopathy, individual proteins of the cardiac system were reconstituted under controlled conditions. Enzymatic data confirmed a diminished calcium sensitivity in the regulation of the cardiac actomyosin system when regulatory protein(s) complex was recombined from diabetic hearts. This diminished calcium sensitivity along with shifts in cardiac myosin heavy chain (V1-->V3) could contribute to the impaired cardiac function in the hearts of chronic diabetic rats. It has also been reported that sarcomeric proteins such as myosin light chain-2 (MLC-2) and troponin I (TnI) could be involved in regulating muscle contraction and in calcium sensitivity. Since phosphorylation of cardiac TnI is associated with altered maximum enzymatic activity and calcium force relationship in isolated muscle preparations. TnI phosphorylation could contribute to depressed myocardial contractility in experimental diabetes. While we have yet to understand the exact function of each component in cardiac muscle and their behavior in concert where all of them act in tandem, we have focussed on the role of contractile proteins and their regulation in diabetes in this review. We have also included a brief discussions on other relevant intracellular components. In summary, there is substantial evidence to suggest that there are independent processes associated with diabetes which effect cardiac performance in experimental animals and in man. The focus of this review has been the explication of a biochemical defect which underlies cardiac contractile dysfunction in experimental models of diabetes.

Animals↗
PubMed1999

Randomised trial of old and new antihypertensive drugs in elderly patients: cardiovascular mortality and morbidity the Swedish Trial in Old Patients with Hypertension-2 study.

BACKGROUND: The efficacy of new antihypertensive drugs has been questioned. We compared the effects of conventional and newer antihypertensive drugs on cardiovascular mortality and morbidity in elderly patients. METHODS: We did a prospective, randomised trial in 6614 patients aged 70-84 years with hypertension (blood pressure > or = 180 mm Hg systolic, > or = 105 mm Hg diastolic, or both). Patients were randomly assigned conventional antihypertensive drugs (atenolol 50 mg, metoprolol 100 mg, pindolol 5 mg, or hydrochlorothiazide 25 mg plus amiloride 2.5 mg daily) or newer drugs (enalapril 10 mg or lisinopril 10 mg, or felodipine 2.5 mg or isradipine 2-5 mg daily). We assessed fatal stroke, fatal myocardial infarction, and other fatal cardiovascular disease. Analysis was by intention to treat. FINDINGS: Blood pressure was decreased similarly in all treatment groups. The primary combined endpoint of fatal stroke, fatal myocardial infarction, and other fatal cardiovascular disease occurred in 221 of 2213 patients in the conventional drugs group (19.8 events per 1000 patient-years) and in 438 of 4401 in the newer drugs group (19.8 per 1000; relative risk 0.99 [95% CI 0.84-1.16], p=0.89). The combined endpoint of fatal and non-fatal stroke, fatal and non-fatal myocardial infarction, and other cardiovascular mortality occurred in 460 patients taking conventional drugs and in 887 taking newer drugs (0.96 [0.86-1.08], p=0.49). INTERPRETATION: Old and new antihypertensive drugs were similar in prevention of cardiovascular mortality or major events. Decrease in blood pressure was of major importance for the prevention of cardiovascular events.

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PubMed1985

[Cardiac involvement in systemic amyloidosis: myocardial scintigraphic evaluation].

To assess the clinical significance of technetium-99m-pyrophosphate (Tc-99m-PYP), -methylene diphosphonate (Tc-99m-MDP) and thallium-201 (Tl-201) myocardial scintigraphy in the diagnosis of cardiac amyloidosis and in the differential diagnosis of cardiac diseases, 12 patients with biopsy-proved systemic amyloidosis (seven with familial amyloid polyneuropathy (FAP) and five with primary amyloidosis) were investigated. The results obtained were as follows: In 10 patients (six with FAP and four with primary amyloidosis) studied by Tc-99m-PYP scintigraphy, two (FAP one, primary amyloidosis one) had diffusely positive myocardial uptake, which was of greater intensity than that of the sternum. Six (four FAP; two primary amyloidosis) also had diffusely positive myocardial uptakes, but the intensity was less than that of the sternum. The remaining two (one FAP; one primary amyloidosis) had only equivocal myocardial uptakes. Two of these patients also had hepatic uptakes and another had both hepatic and thyroid uptakes. The intensity of myocardial uptake of Tc-99m-PYP in patients with echocardiographic left ventricular hypertrophy and/or highly refractile myocardial echoes, so-called granular sparkling appearance (GS) was slightly greater than that in patients with neither myocardial hypertrophy nor GS. FAP had slightly less intensity than primary amyloidosis. In 29 persons with other cardiac diseases and normal subjects examined by Tc-99m-PYP scintigraphy, seven (two dilated cardiomyopathy; two sarcoidosis; three hypertensive heart disease) also had diffusely positive myocardial scans of mild or moderate degree. However, none of them had marked myocardial or other tissue uptakes. Both Tc-99m-PYP and -MDP scintigraphic studies were performed in four patients (three FAP; one primary amyloidosis). In Tc-99m-MDP scintigraphy, diffusely positive myocardial uptakes were observed in two patients with FAP and the remaining two had negative scans. The intensity of Tc-99m-MDP myocardial uptake in each patient was significantly lower than that of Tc-99m-PYP uptake. Tl-201 scintigraphy was carried out in 10 patients (six FAP; four primary amyloidosis). Left ventricular hypertrophy was found in six patients and right ventricular visualization in five. Although electrocardiograms in seven of 10 patients showed QS patterns in the right to mid precordial leads, similar to that seen in antero-septal and extensive anterior myocardial infarctions, neither myocardial perfusion defect nor low uptake on Tl-201 images was detected in nine of them. The scintigrams in another one, which showed low uptake at the apical portion of the left ventricle, were considered normal.(ABSTRACT TRUNCATED AT 400 WORDS)

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PubMed2000

Pathology and pathogenesis of arrhythmogenic right ventricular cardiomyopathy.

Arrhythmogenic right ventricular cardiomyopathy is a primary heart muscle disease characterized by progressive myocardial atrophy of the right ventricle, with transmural fatty or fibrofatty replacement, either segmental or diffuse, accounting for electrical instability at risk of life-threatening ventricular arrhythmias. It was recently included among cardiomyopathies in the revised WHO classification. The disease was found to be a major cause of sudden death in the young and in athletes of the Veneto Region, Italy. A familial occurrence with autosomic dominant inheritance was then discovered with a prevalence estimated to be 6/10,000 inhabitants and 5 loci have been identified by linkage analysis so far, 2 mapping to chromosome 14 and to chromosome 1, 2 and 3 one each. A recessive form associated with palmoplantar keratosis has also been reported, mapping to chromosome 17. Nonetheless, the specific gene defects as well as the defective coded proteins have not yet been identified. At gross examination, the right side of the heart appears yellowish or whitish as to suggest a fatty or fibrofatty infiltration of the underlying myocardium; the myocardial loss frequently accounts for a parchment like, translucent look of the right ventricular free wall. Aneurysms of the right ventricular free wall, whether single or multiple, were reported in about 50% of cases in a recent pathologic investigation, and are considered a pathognomonic feature of arrhythmogenic right ventricular cardiomyopathy; they are typically located in the inferior, diaphragmatic wall, underneath the posterior leaflet of the tricuspid valve, as well as in the infundibulum and at the apex. Right ventricular enlargement, whether mild, moderate or severe, is a constant feature. Involvement of the left ventricle has been reported in almost 50% of cases. At histology, the pathologic process generally starts from the subepicardium and extends to the endocardium in a wave-front phenomenon. The residual, spared myocytes are located within the subendocardial trabeculae and few myocardial fascicles are scattered throughout the fibrofatty tissue. All stages of myocardial injury and repair are recognizable: acute cell death with sarcolysis and inflammatory infiltrates; subacute damage with "active fibrosis", including dying myocytes, lymphocytes and macrophages, or otherwise adipocytes replacing vanished myocytes; and, eventually, chronic stage with fibrous tissue and adipocytes surrounding residual surviving myocytes. Both the etiology and pathogenesis of arrhythmogenic right ventricular cardiomyopathy are still unknown. In particular, the mechanisms leading to progressive loss of myocardium and fibrofatty replacement are speculative. According to the frequent finding of inflammatory infiltrates at histology, an inflammatory theory has been advanced and infective, toxic or immune mechanisms have been investigated. Recently, apoptosis has been documented both in autoptic and bioptic material, suggesting that recurrent bouts of apoptosis may account for progressive atrophy of the myocardium which is then replaced by fibrofatty tissue. Apoptosis may be triggered by T-lymphocytes.

Apoptosis↗
PubMed2006

Impact of statin therapy at discharge on 1-year mortality in patients with ST-segment elevation myocardial infarction treated with primary angioplasty.

BACKGROUND: Statin therapy can reduce long-term mortality in several subgroups of patients with coronary artery disease, but the benefits after primary angioplasty for ST-segment elevation myocardial infarction (STEMI) have yet to be established. The aim of the current study was to determine whether statin therapy is associated with a reduction in mortality in patients with STEMI treated with primary angioplasty. METHODS: Our population is represented by a total of 1513 consecutive in-hospital survivors treated with primary angioplasty for STEMI between April 1997 and October 2001. Patients were divided in two groups according to statin therapy (statin group, n=893; control group, n=620) at discharge. Clinical follow-up was performed at 1 year. A propensity score, built on the basis of variables independently associated with statin prescription, was used to investigate the benefits from statin therapy in subgroups of patients that were homogeneous in terms of baseline clinical and angiographic characteristics. RESULTS: At 1-year follow-up statin therapy was associated with a significantly lower mortality (1.2% versus 7.1%, R(2) [95% CI]=0.16 [0.09-0.32], p<0.0001). These benefits were confirmed in all subgroups according to the propensity score, and at multivariate analysis (adjusted R(2) [95% CI]=0.24 [0.12-0.47], p<0.0001). CONCLUSIONS: Statin therapy at discharge was associated with a significant reduction in 1-year mortality after primary angioplasty for STEMI. Therefore, the use of statins is highly recommended in these patients.

Aged↗
PubMed2000

Effects of acute hyperglycaemia on cardiac function: an echocardiographic study of monozygotic twins.

BACKGROUND: A major cause of morbidity in type I diabetes is congestive heart failure due predominantly to left ventricular diastolic dysfunction. The mechanism of diastolic dysfunction remains unknown and does not relate to blood pressure, microvascular complications and glycated haemoglobin. Hyperglycaemia is the hallmark of diabetes and is a potential determinant of left ventricular diastolic dysfunction. OBJECTIVE: To determine whether acute hyperglycaemia can induce changes in left ventricular diastolic function in normal subjects similar to those observed in insulin-dependent diabetes mellitus (IDDM). DESIGN: Cross-sectional study. SETTING: London teaching hospital. SUBJECTS: Sixteen twins from eight identical twin pairs discordant for IDDM (age 18-38 years, five male) were studied; none had a history or evidence of myocardial ischaemia, valvular or primary heart muscle disease, systemic hypertension or nephropathy. INTERVENTIONS: Non-diabetic twins underwent a hyperglycaemic clamp at 10 mmol/l. MAIN OUTCOME MEASURES: Doppler echocardiography was performed in basal condition in identical twin pairs discordant for IDDM and repeated in the non-diabetic twins during hyperglycaemia. Blood glucose, insulin and catecholamines were measured at baseline and during hyperglycaemia. RESULTS: Transmitral Doppler E/A velocity ratio was significantly lower in diabetic than non-diabetic twins at baseline (1.44 (0.38) vs. 1.51 (0.19), P<0.05). Glucose infusion in the non-diabetic twins resulted in an increase in their E/A ratio (1.51 (0.19) vs. 1.82 (0. 47), P<0.05) due to an increase in E velocity (68 (12) to 64.7 (10. 7), P<0.05) and a decrease in the peak A velocity (42.7 (3.85) to 38. 0 (4.1), P<0.05). No significant changes were observed in peak E velocity or isovolumic relaxation time in the non-diabetic twins between baseline and hyperglycaemia. CONCLUSIONS: The alterations in left ventricular diastolic function induced by acute hyperglycaemia and consequent increase in plasma catecholamines do not mimic those demonstrated in IDDM patients.

Adolescent↗
PubMed1995

Suppressed fibrinolysis after administration of low-dose aprotinin: reduced level of plasmin-alpha2-plasmin inhibitor complexes and postoperative blood loss.

Various clinical investigation have shown that aprotinin therapy reduces bleeding after open-heart operations. In this study low-dose aprotinin, 30,000 KIU/kg in the cardiopulmonary bypass (CPB) priming volume and 7,500 KIU/kg intravenously each hour during CPB, was used in ten patients undergoing primary myocardial revascularization or surgery for valvular diseases. Another ten patients served as controls. Blood loss, platelet count and plasma levels of hemoglobin, antithrombin III, fibrinogen, fibrinogen degradation products (FDP), total plasmin inhibitor and alpha2-plasmin inhibitor-plasmin complexes were evaluated at nine preoperative, intraoperative and postoperative points. Intraoperative and postoperative blood loss was significantly reduced in the aprotinin group. There was no significant difference between the two groups in platelet count and levels of hemoglobin and antithrombin III. A significant increase in FDP during CPB in the control group indicated hyperfibrinolysis. The levels of plasmin inhibitor were significantly reduced during CPB in the control group. The alpha 2-plasmin inhibitor-plasma complex levels, indicating the plasmin activity, were significantly reduced in the aprotinin group. These results confirmed that low-dose aprotinin reduced blood loss with the prevention of hyperfibrinolysis during CPB and demonstrated improved hemostasis.

Antifibrinolytic Agents↗
PubMed2004

Management of dyslipidaemia in HIV-infected patients receiving antiretroviral therapy.

Dyslipidaemia associated with the treatment of HIV infection, particularly with the use of protease inhibitors (PIs), can raise cholesterol and triglyceride (TG) levels to the thresholds indicated for intervention. Recent evidence from epidemiological studies has shown that there are correlations between antiretroviral drug use and increased risks for, and incidences of, cardiovascular disease, including myocardial infarction and coronary heart disease. The primary goals of dyslipidaemia therapy for HIV patients are reductions of both low-density lipoprotein cholesterol (LDL-C) and markedly elevated TG levels. Dietary strategies and exercise programs may be tried, although these have shown inconsistent results. The two options for drug therapy are switching antiretroviral agents and using lipid-lowering drugs. Each approach is associated with advantages and limitations, and the need to maintain viral suppression must be balanced with the need to treat abnormal lipid levels. Most drug switches replace the PI component with drugs from another antiretroviral class. Selection of drug therapy for lipid lowering depends on the type of dyslipidaemia predominating and the potential for drug interactions. The use of the statins pravastatin and atorvastatin is recommended for the treatment of patients with elevated LDL-C levels and gemfibrozil or fenofibrate for patients with elevated TG concentrations. Development of new PIs with more favourable effects on the lipid profile should be of benefit.

Antiretroviral Therapy, Highly Active↗
PubMed1991

Diabetes mellitus in sand rats (Psammomys obesus): microangiopathy during development of the diabetic syndrome.

The purpose of the study was to investigate the development of microangiopathic complications in North African sand rats with diabetes induced by a long-term standard laboratory diet. Hyperinsulinaemic rats, whether non-diabetic obese or diabetic, developed capillary basement membrane (CBM) thickening in the skin; in insulin-dependent animals, this change was diffuse. Many PAS positive areas were demonstrated in skeletal muscle and myocardium, together with evidence of microangiopathy; the primary myocardial lesion in insulin-dependent disease was ischaemic fibrosis. The kidney was also affected with marked basement membrane thickening in Bowman's capsule and glomerular capillaries; glomerulosclerosis and tubular changes were found in insulin-dependent disease. No evidence of diabetic retinopathy was found, and there was a high incidence of cataract.

Animals↗
PubMed1983

[Involvement of the thoracic was in algodystrophy. Apropos of a case report].

With reference to an unusually severe and extensive case of algodystrophia, the sternal and costal localizations of this disorder are described. These fit the definition of the painful anterior thoracic wall syndrome, described i 1955 by Printzmetal and Massumi, which may complicate chronic coronary insufficiency or myocardial infarction or occur as a primary disease.

Bone Diseases, Metabolic↗
PubMed2002

Diastolic subclinical primary alterations in Marfan syndrome and Marfan-related disorders.

BACKGROUND: The extracellular matrix tissue of the myocardium importantly contributes to left ventricular (LV) performance. Inherited connective tissue disorders related to the FBN1 gene could involve cardiac interstitium resulting in functional abnormalities. HYPOTHESIS: To disclose a primary involvement of myocardium, LV function was studied in 28 patients affected by Marfan syndrome or Marfan-related disorders: 20 Marfan and 8 MASS (Mitral valve prolapse, Myopia, Aortic dilatation, Skeletal involvement, Skin striae) and in 28 healthy, age and gender-matched controls. No valvular regurgitation or any other cardiac alterations were present. METHODS: Echocardiographic study was performed to investigate LV systolic and diastolic function. RESULTS: No statistically significant differences were observed between patients and the control group in LV dimensions, systolic function parameters (ejection and shortening fraction), and some diastolic function parameters (E peak, A peak, E/A), while statistically significant differences were found between patients and the control group in LV mass (128.7 +/- 46.6 vs. 83.7 +/- 14.5 g/m2, p<0.008), in isovolumic relaxation time (102.0 +/- 24.0 vs. 80.1 +/- 11.2 ms, p<0.016), and in deceleration time of the E wave (127.5 +/- 19.3 vs. 208.6 +/- 24.5 ms, p<0.001) and the A wave (66.4 +/- 8.2 vs. 87.5 +/- 23.4 ms, p <0.008). CONCLUSIONS: These data show an unusual pattern of transmitral diastolic flow in which a decreased ventricular compliance and reduced myocardial relaxation coexist. Thus, in Marfan syndrome and in Marfan-related disorders, subclinical diastolic alterations are present independent of valvular disease and might represent an early marker of primary myocardial involvement.

Adult↗
PubMed1995

Vascular selective calcium entry blockers in the treatment of cardiovascular disorders: focus on felodipine.

Calcium entry through L-type calcium channels is essential for contraction of both arterial smooth muscle and the myocardium, and is important in cardiac conduction. First-generation calcium entry blockers lack or have a modest degree of vascular selectivity and inhibit cardiac function at doses producing therapeutic arterial dilatation. Such agents may cause deterioration in patients with left ventricular dysfunction, and their combination with a beta-adrenergic blocker may adversely affect cardiac contractility and conduction. Development of newer agents has focused on obtaining a higher degree of vascular selectivity. Felodipine is a highly vascular selective calcium entry blocker, with a vascular selectivity ratio greater than 100, as shown experimentally. Isradipine and nicardipine are also vascularly selective calcium entry blockers. Hemodynamic studies in patients with hypertension, coronary artery disease, congestive heart failure, or in patients receiving beta-adrenergic blockade, show that felodipine can produce profound arteriolar dilatation without the negative effects of left ventricular systolic performance. Furthermore, felodipine alone or when added to a beta-adrenergic blocker does not interfere with cardiac conduction. The primary mechanism that accounts for the efficacy of dihydropyridine calcium entry blockers in hypertension and angina pectoris is arterial dilation, whereas nondihydropyridines may also derive part of their effect from inhibition of cardiac performance. As some of these patients, most commonly the elderly, have concomitant left ventricular dysfunction, it should be advantageous to avoid myocardial depression in the treatment of their primary disease. Preliminary studies in patients with heart failure indicate that felodipine and amlopidine may improve hemodynamics, reduce neurohormonal activation, and increase exercise tolerance, but final conclusions must await the randomized clinical trials now underway.

Amlodipine↗
PubMed2004

Single vs multivessel treatment during primary angioplasty: results of the multicentre randomised HEpacoat for cuLPrit or multivessel stenting for Acute Myocardial Infarction (HELP AMI) Study.

DESIGN: Prospective randomized, multicentre study. RATIONALE: Recanalisation of the culprit lesion is the main goal of primary angioplasty for acute myocardial infarction. With the exception of cardiogenic shock, staged procedures are performed in the presence of multivessel disease. The study hypothesis is that with modern non-thrombogenic stents (heparin coated) complete revascularization with multivessel treatment can be safely achieved during the primary angioplasty procedure with a lower need of subsequent revascularization procedures and at a lower cost. ENDPOINTS: PRIMARY: 12-month incidence of repeat revascularization (any revascularization, infarct related artery as well as non-infarct-related artery). SECONDARY: (1) in hospital repeat revascularization, reinfarction and death; (2) total hospital cost (including a 12 months follow-up period). METHODS: 69 patients with ST elevation Acute Myocardial Infarction (AMI), <12 hours after symptoms onset, undergoing primary angioplasty, with documented multivessel disease and both culprit lesion and 1 to 3 other lesions suitable for stent implantation. Unbalanced randomization between culprit lesion treatment only (n = 17) and complete multivessel treatment (n = 52, with 71 additional lesions treated). RESULTS: The two groups were well balanced in terms of clinical characteristics, number of diseased vessels and angiographic characteristics of the culprit lesion. In the complete multivessel treatment group 2.36 +/- 0.64 lesions per patient were treated using 2.73 +/- 0.78 heparin coated stents (1.00 lesions and 1.29 +/- 0.61 stents in the culprit treatment group, both p < 0.001). The duration of the procedure increased from 53 +/- 21 min (culprit treatment group) to 69 +/- 32 min (p = 0.032) and the amount of contrast used from 242 +/- 102 ml (culprit treatment group) to 341 +/- 163 ml (multivessel complete treatment), p = 0.025. A similar low incidence of in-hospital major adverse cardiac events was observed in the 2 groups (0 and 3.8% in culprit and multivessel treatment groups, p = 0.164). The increase in the incidence of new revascularisation in the culprit treatment group at 12 month follow-up was not significant (35 vs 17%, p = 0.247) but was sufficient to compensate the initial higher in-hospital cost, with a similar 12 month hospital cost in the 2 groups (Euro 22,330 +/- Euro 13,653 vs Euro 20,382 +/- Euro 11,671, p = 0.231). CONCLUSION: Multivessel treatment during primary PTCA was safe in this controlled trial. However, when only the culprit lesion was initially treated, the need for subsequent clinically driven revascularization remained low and no clinical or economical advantages were obtainable with a more aggressive initial approach. In clinical practice, a staged approach to multivessel treatment during primary angioplasty avoids to treat unnecessarily non clinically relevant lesions.

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