Risk stratification in acute coronary syndrome: focus on unstable angina/non-ST segment elevation myocardial infarction.

Although there have been advances in the management of unstable angina/non-ST segment elevation myocardial infarction syndromes, the rate of cardiovascular mortality after discharge is still unacceptably high. With many therapeutic options available, the clinician is challenged to identify the safest and most effective treatment for long term survival of each individual patient

Acute myocardial infarction caused by amphetamines: a case report and review of the literature.

Cardiotoxicity manifesting as myocardial ischemia is not generally recognized as a side effect of amphetamine use or abuse. However, at least 9 cases have been reported since 1987. In this report a case of acute myocardial infarction due to oral amphetamine therapy is presented. The patient was treated with thrombolytic therapy but there were no signs of reperfusion. His coronary cine-angiograms were normal. The literature regarding amphetamine use or abuse is also reviewed, and the possible mechanisms of this pathology are analyzed.

Thrombosis of a mitral valve prosthesis resulting from Staphylococcus epidermidis endocarditis.

A 70-year-old man with a Duromedics mitral valve prosthesis had two episodes of infective endocarditis caused by enterococcus (1994 and 1996). Colonoscopy revealed five polyps. Surgical resection was performed and 2 days later the patient had dyspnea and fever. Because of a suspected valve thrombosis, intravenous heparin was given which resulted in hematic effusion in the Douglas' cul-de-sac. Intravenous heparin was withdrawn but the patient continued to have a worsening dyspnea, hyperthermia and hypotension. The patient was transferred to our Institution in cardiogenic shock. Acute thrombosis of the valve was diagnosed by echocardiography, and the patient died before transesophageal Doppler echocardiography was performed. Post mortem examination revealed mitral valve infective thrombosis. In patients with valvular prostheses, endocarditis is an added thromboembolic risk.

[Effects of reperfusion and coronary reocclusion on the variability of heart rate in patients with acute myocardial infarction]. / Influenza della riperfusione e della riocclusione coronarica sulla variabilità della frequenza cardiaca in pazienti con infarto miocardico acuto.

The aim of this study was to analyze the very early (first 24 hours) effect of successful or failed thrombolytic therapy on the autonomic nervous system. Thirty consecutive patients with a first acute myocardial infarction were enrolled in the study, and admitted to the Coronary Care Unit within 6 hours of the onset of symptoms and treated with systemic thrombolytic therapy. All patients underwent 24-hour Holter monitoring in order to analyze ST segment variation. The autonomic nervous system was evaluated by frequency-domain heart rate variability: low frequency/high frequency ratio (LF/HF) was measured at the beginning of Holter monitoring (T1), 15 min after reperfusion or 1 hour from the start of thrombolytic therapy (T2) and after 24 hours (T3). Reperfusion status was assessed by a > or = 50% reduction in ST segment elevation within 90 min of thrombolytic therapy, and early CK-MB peak. Early coronary reocclusion was detected by early reduction in ST segment elevation followed by stable ST segment re-elevation. Twenty patients (66%) showed successful thrombolytic therapy (Group 1), 5 patients (17%) had no evidence of successful thrombolytic therapy (Group 2) and 5 patients (17%) showed an early reocclusion (Group 3). LF/HF ratio values at T1 were similar in the three groups (5.66 +/- 1.7 vs 5.65 +/- 1.2 vs 5.51 +/- 0.9, NS). At T2, LF/HF ratio was significantly higher in Group 1 and 3 than Group 2 patients (9.21 +/- 1.7 and 11.1 +/- 1.2 vs 5.58 +/- 1.4, respectively, p < 0.001). In Group 1 LF/HF ratio was significantly lower at T3 when compared with T1 and T2 (1.9 +/- 1 vs 5.66 +/- 1.7 and 9.21 +/- 1.7, respectively, p < 0.001). Conversely, in Group 3 LF/HF ratio at T3 was similar to values measured at T1 (5.59 +/- 1.7 vs 5.51 +/- 0.9, respectively, NS) and significantly higher than those detected in Group 1. In Group 2, LF/HF ratio resulted substantially unchanged at T3 (5.49 +/- 1.7, NS). In conclusion, 1) successful thrombolytic therapy induces early beneficial effects on the autonomic nervous system function, as shown by increased heart rate variability values, when compared with failed thrombolytic therapy; 2) however, during the early period following coronary reperfusion, a transient but dramatic increase in sympathetic activity is observed. This could trigger coronary flow instability, thus facilitating reocclusion, by activating different pathogenetic mechanisms (increased vascular tone, platelet activation, thrombogenic factor prevalence); 3) early coronary vessel reocclusion precludes favorable effects of reperfusion on sympatho-vagal balance observed after the first 24 hours.

Left ventricular metastasis from uterine leiomyosarcoma.

Cardiac metastases are uncommon but seem to be increasing in incidence, possibly in relation to prolonged survival of cancer patients. Leiomyosarcoma metastatic to the heart is extremely rare. We report the case of a 57-year-old woman previously treated for uterine leiomyosarcoma who presented with dyspnea, electrocardiographic changes mimicking myocardial infarction, and normal enzymes. A left intraventricular mass, suspected as cardiac metastasis, was revealed by echocardiography. The patient died 1 week later. At autopsy the mass proved to be histologically a metastasis of the uterine tumor.

Unstable angina: prognosis of the individual patient.

Not all patients diagnosed with unstable angina have the same outcome. Thus, it is incumbent on the physician caring for these patients to try to identify factors that will risk-stratify them. These factors include the degree of coronary angiographic stenosis, the lesion morphology, severity of symptoms, presence or absence of transient myocardial ischemia, and state of left ventricular function. In addition, many other factors including the patient's age, gender, and coexisting medical disorders must be considered when trying to prognosticate an individual patient. Clinical experience indicates that clinical indices that combine information provided by all of the above related variables should have more powerful prognostic significance than any individual variable.

Relationship between plasma endothelin-1 levels and myocardial ischemia induced by exercise testing.

At peak exercise, plasma endothelin-1 concentration increases in patients with effort angina as well as thallium-201 radionuclide perfusion defects; the opposite occurs in patients with normal scans and in healthy volunteers. It is concluded that exercise-induced ischemia correlates with enhanced endothelin-1 production.

[The correlation between the clinical characteristics and psychological status in syndrome X patients]. / Correlazione tra caratteristiche cliniche e stato psicologico in pazienti con sindrome X.

Patients with anginal symptoms and normal coronary arteries have been found to present with high levels of neuroticism i.e. anxiety, depression and somatic concerns. Whether neuroticism plays a role in precipitating coronary hypoperfusion and symptoms is still a matter of investigation. The present study was undertaken to assess the relation between psychological status and clinical symptoms in 22 patients with syndrome X (angina and ST depression with angiographically normal coronary arteries and reversible myocardial perfusion abnormalities). Neuroticism was evaluated by Beck Depression Inventory, Hamilton Anxiety Rating Scale (HAM-A), State-Trait Anxiety Inventory, Sheehan Patient Rated Anxiety Scale, State-Trait Anger Expression Inventory (STAXI), Brief Psychiatric Rating Scale and Clinical Global Impression. Data were compared with those obtained in 30 patients with stable angina as well as coronary artery disease. All patients underwent an exercise stress testing and a 24-hour ambulatory Holter monitoring. Patients with syndrome X scored significantly higher than stable angina (p < 0.05 each) on all psychological tests but STAXI. No significant differences, between syndrome X and stable angina were found in exercise stress testing parameters and during Holter monitoring. Twelve out of 22 syndrome X patients had a score > 28 in HAM-A (Group 1, with frank psychiatric abnormalities). The remaining 10 patients were labelled as Group 2. No significant differences between Group 1 and Group 2 were found in exercise capacity (time to 0.1 m V ST depression: 397 +/- 73 and 419 +/- 137 s, respectively; NS) or in the number of anginal episodes per day (0.9 +/- 1.3/24 hours and 0.6 +/- 0.8/24 hours respectively; NS). In contrast, Holter monitoring showed a significantly higher number of ischemic episodes in Group 1 than in Group 2 (1.6 +/- 1.7 vs 0.1 +/- 0.3/24 hours; p < 0.02) and a greater duration of ischemia (23.8 +/- 32 vs 0.3 +/- 1 min/24 hours; p < 0.03). We conclude that: patients with syndrome X evidence elevated neuroticism scores; a high degree of anxiety correlates with increased transient myocardial ischemia during daily life; neuroticism may itself cause changes in coronary microvascular function in syndrome X. Alternatively it may simply modulate the threshold for ischemia in the presence of underlying dysfunction.

Transient sympathovagal imbalance triggers "ischemic" sudden death in patients undergoing electrocardiographic Holter monitoring.

OBJECTIVES: The aim of this study was to investigate the relation between "ischemic" sudden death (arrhythmic death preceded by ST segment shift) and autonomic nervous system activity. Background. Mechanisms precipitating sudden death are poorly known despite the importance of detecting functional factors that may contribute to such a fatal event. METHODS: We analyzed the tapes of eight patients (seven men and one woman with a mean age of 66 +/- 8 years) who had ischemic sudden death during ambulatory electrocardiographic (Holter) monitoring. Four patients had unstable and four had stable angina; none was taking antiarrhythmic drugs. Twenty patients with angina and transient myocardial ischemia during Holter monitoring served as control subjects. Arrhythmias, ST segment changes and heart rate variability were analyzed by a computerized interactive Holter system. RESULTS: Five patients had ventricular tachyarrhythmias (ventricular fibrillation in three, ventricular tachycardia in two), and three had bradyarrhythmias (atrioventricular block in two, sinus arrest in one) as the terminal event; all eight patients showed ST segment shift (maximal change 0.46 +/- 0.16 mV; with ST elevation in two) that occurred 41 +/- 34 min (mean +/- SD) before sudden death. The standard deviation of normal RR intervals (SDNN) was 89 +/- 33 ms during the 10 +/- 6 h of Holter monitoring; 5 min before the onset of the fatal ST shift, SDNN measurements were significantly lower than during the initial 5-min period (48 +/- 10 vs. 29 +/- 9 ms; p=0.002). In control patients, the SDNN was 102 +/- 39 ms during Holter monitoring, whereas it measured 56 +/- 30 ms 5 min before the most significant episode of ST shift (p<0.01 vs. 29 +/- 9 ms [corrected] in the group with sudden death). CONCLUSIONS: Autonomic dysfunction, as detected by a marked decrease in heart rate variability, is present in the period (5 min) immediately preceding the onset of the ST shift precipitating ischemic sudden death. These data suggest that sympathovagal imbalance may trigger fatal arrhythmias during acute myocardial ischemia, thus resulting in sudden death.

[The noninvasive identification of patients with angina and normal coronary arteries]. / Riconoscimento non invasivo dei pazienti con angina a coronarie normali.

BACKGROUND: Although patients with syndrome X (angina and normal coronary arteries, in absence of coronary spasm, cardiomyopathy or valvulopathy) and those with stable angina as well as documented coronary artery disease share a similar clinical presentation (effort related symptoms, positive exercise stress testing and reversible perfusion defects), their prognosis is markedly different. Coronary atherosclerosis is usually progressive relative to morbidity and mortality. Conversely prognosis both in terms of persistence of pain and mortality appears to be benign in syndrome X. Most cardiologists favor proceeding with coronary angiography in all patients presenting with exercise induced ST depression and reversible perfusion defects. However, it should not be assumed that this strategy will remain the preferred one. The aim of this study was to assess whether non invasive testing could identify underlying coronary artery anatomy, thus prognosis in the above subset of patients. The approach was selected on a clearly stated objective of how isosorbide dinitrate and verapamil may influence coronary flow reserve, thus exercise stress testing in syndrome X. Nitrates have been shown to reduce coronary flow reserve during stress tachycardia. The opposite occurs with calcium blockers. METHODS: We studied 48 patients with effort angina referred to our laboratory for diagnostic evaluation. All patients underwent two separate sessions at one-day interval. Each session consisted of exercise stress testing before and after isosorbide dinitrate (s.l.; 5-10 mg) or verapamil (i.v.; 10 mg), given in a randomized crossover fashion. Angiography was performed within 3 months from testing. Efficacy of drugs in terms of exercise capacity was assessed by using the following criteria: 1) prevention of significant (> or = 0.1 mV) ST depression while reaching same workload levels attained during baseline testing; 2) improvement in the ischemic thresholds, that is an increase in: time to 0.1 mV ST depression > or = 120 sec., with heart rate (> or = 10 bpm) and rate pressure product (> or = 2 U x 1000) greater than those attained during baseline testing; 3) increase in time to peak exercise (> or = 120 sec). RESULTS: In syndrome X, both drugs resulted ineffective in one patient, one patient showed a favourable response to isosorbide dinitrate whereas the remaining 13/15 patients improved exercise capacity following verapamil, but not isosorbide dinitrate. The opposite occurred in coronary artery disease patients: both isosorbide dinitrate and verapamil were effective in 21/33 patients, and ineffective in 8/33 patients. The remaining 4 patients responded to isosorbide dinitrate but not to verapamil. CONCLUSIONS: 1) Verapamil, but not isosorbide dinitrate, improves exercise capacity in syndrome X; 2) this does not apply to patients with stable angina; 3) a favourable response to verapamil but not to isosorbide dinitrate is both a sensitive (86%) and specific (100%) method for identifying patients with angina and normal coronary arteries; 4) non invasive testing may select those effort angina patients who have to proceed directly to coronary angiography; 5) some patients with effort related angina may not require further investigation.

[A transient decrease in heart rate variability in patients with sudden "ischemic" death during Holter monitoring]. / Riduzione transitoria della variabilità della frequenza cardiaca in pazienti con morte improvvisa "ischemica" durante Holter.

BACKGROUND: Mechanisms precipitating sudden death are poorly known, in spite of the importance to detect functional factors which may contribute to such fatal event. Aim of the study was to investigate the relationship between "ischemic" sudden death (ISD: arrhythmic death preceded by acute myocardial ischemia) and autonomic nervous system activity. METHODS: We analysed the tapes of 6 patients (pts) (5 males; 67 +/- 12 yrs) suffering ISD during Holter monitoring (HM). One pt had recent onset angina, 2 had unstable and 3 stable angina; none was taking antiarrhythmic drugs. Arrhythmias, ST segment and heart rate variability (HRV) were analysed by a computerized interactive HM system, in order to obtain data on transient ischemia and sympatho-vagal balance. RESULTS: Five pts showed ventricular tachyarrhythmias (2 VF, 3 VT), and 1 had a bradyarrhythmia (advanced A-V block) as the terminal event; all pts showed ST shift (max: 0.37 +/- 0.28 mV; 1 with ST elevation; 4 with anginal pain) 53 +/- 35 min before ISD. SD of normal R-R intervals (SDNN) was 112 +/- 26 msec in the 11 +/- 8 hrs of HM, whereas it was 97 +/- 48 msec in the initial hour and 59 +/- 21 msec in the initial 5 min segment. Measurements of SDNN showed a marked decrease 5 min before the onset of fatal ischemic ST shift: 32 +/- 14 msec (p = 0.003). Also, pNN50 (percent of adjacent R-R differing > 50 msec: marker of vagal activity) was significantly reduced before ISD, when compared to the initial 5 min segment (from 10 +/- 5 to 7 +/- 4%; p < 0.03). Such changes were not observed before uncomplicated (that is not associated with malignant arrhythmias) ST shift episodes during HM. CONCLUSIONS: Autonomic dysfunction, as detected by a marked decrease of HRV, is present in the period (5 min) immediately preceding the onset of ST shift precipitating ISD; simultaneous measurements of vagal signals showed similar changes. These data suggest that sympatho-vagal unbalance may trigger fatal arrhythmias during acute myocardial ischemia, hence resulting in ISD.

Relation of severity of symptoms to transient myocardial ischemia and prognosis in unstable angina.

OBJECTIVES: This study was undertaken to compare the relative power of the severity of angina versus that of any other clinical, electrocardiographic (ECG) and angiographic findings in predicting the risk of subsequent in-hospital coronary events in patients admitted to the coronary care unit for treatment of unstable angina. BACKGROUND: The presence or absence of chest pain has traditionally been used to guide management and therapy of unstable angina. However, recent studies raised the possibility that the cumulative duration of ischemia may be an additional index of prognosis. METHODS: We studied 104 consecutive patients admitted to the coronary care unit because of unstable angina. Diaries of symptoms were accurately kept. All patients underwent Holter ambulatory ECG monitoring during the 1st 24 h and angiography within 1 week of admission. RESULTS: During the hospital stay, 41 patients (group 1) had subsequent coronary events; the remaining 63 patients (group 2) had a good clinical outcome. Recurrence of chest pain after admission was observed in 76% of patients: 36 of the 41 group 1 patients (sensitivity 88%) and 43 of the 63 group 2 patients (specificity 32%). Anginal scores (frequency and persistence of pain, duration of each single episode and pain-free interval) showed high specificity but low sensitivity for detecting evolution toward subsequent coronary events. On Holter monitoring, the duration/24 h of the total number of ischemic episodes was consistently greater in group 1 than in group 2. A cumulative duration of ischemia > or = 60 min/24 h was observed in 34 of the 41 group 1 patients (sensitivity 83%) but in only 16 of the 63 group 2 patients (specificity 75%). High risk coronary artery lesions (left main coronary artery disease or complex stenosis) were detected in 36 of the 41 group 1 patients and in 26 of the 63 group 2 patients. CONCLUSIONS: Transient myocardial ischemia detected by Holter monitoring, but not chest pain, is the best predictor of unfavorable short-term clinical outcome. The decision to perform early angiography and revascularization cannot be based on symptoms alone.

[Myocardial infarct with normal coronary vessels: an association with dysfunction of the coronary microcirculation]. / Infarto miocardico con coronarie normali: associazione con la disfunzione del microcircolo coronarico.

The association of acute myocardial infarction (AMI) with normal coronary arteries was analyzed prospectively. A series of 128 consecutive patients underwent coronary angiography within 1 week from AMI. Seven patients, all females, had no coronary artery lesions and were considered eligible for the study. All 7 patients underwent atrial pacing (10 g/min increments every 2 min), ergonovine testing (E; total dose 0.650 mg i.v.). Great cardiac vein flow (GCVF; thermodilution technique), mean aortic pressure (MAP), anterior coronary resistance (ACR) and myocardial lactate extraction [(Lac art-Lac gcv)/Lac art] were measured at baseline and during testing. Pacing-induced typical chest pain occurred in 5 patients: 4 of them showed concurrent significant (> or = 0.15 mV) ST downsloping. At peak pacing, GCVF increased only by < 50%, or even decreased, in all patients. Baseline lactate extraction (0.13 +/- 0.11) changed to lactate production (-0.15 +/- 0.10) in 7/7 patients. None of the patients showed focal epicardial coronary artery spasm following E. During testing, however, all 7 patients showed decrease in GCVF (110 +/- 47 versus 74 +/- 21; p < 0.005), increase in ACR (0.92 +/- 0.29 versus 1.43 +/- 0.20; p < 0.001), and significant coronary lactate production (-0.18 +/- 0.12). Six patients referred slight to moderate chest pain, which was accompanied by ST downsloping in 4.(ABSTRACT TRUNCATED AT 250 WORDS)

[Exudative pericarditis with pleural plaques caused by exposure to asbestos, resolved with steroidal treatment]. / Pericardite essudativa associata a placche pleuriche da esposizione all'asbesto, risolta da trattamento steroideo.

We report a case of a 73-year old railwayman with an asymptomatic large pericardial effusion diagnosed by a routine echocardiogram. By clinical and laboratory tests we excluded an immune, infectious, tuberculous and neoplastic origin of the pericardial effusion. A computed tomography scan of the thorax showed left pleural plaques. Pleural and pericardial biopsies showed fibrohyaline plaques and diffuse aspecific, chronic inflammation consistent with asbestos exposure. By using steroid treatment there was no further evidence of pericardial inflammation or pericardial effusion at 8 month follow-up. Steroid drugs are therefore suggested as a first choice treatment in patients with pleuropericardial effusion as well as chronic asbestos exposure.

[Cardiac tamponade and rheumatoid arthritis: medical approach or pericardiectomy?]. / Tamponamento cardiaco e artrite reumatoide: approccio medico o pericardiectomia?

The authors report the case of a sixty-seven-year-old man with seronegative rheumatoid arthritis since 1967. After the treatment was discontinued, a symptomatic pericardial effusion developed during an exacerbation of rheumatoid arthritis. Histological findings suggested a rheumatoid origin. Consecutive pericardiocentesis and a concomitant adequate treatment resolved cardiac tamponade, at least during short-term follow-up. However, a long term observation will be necessary to exclude recurrent effusion or evolutive constrictive pericarditis.

[An analysis of the variability of the heart rate and its significance in the risk stratification of patients with unstable angina]. / Analisi della variabilità della frequenza cardiaca e suo significato nella stratificazione di rischio dei pazienti con angina instabile.

Decreased heart rate variability (HRV) correlates with increased sympathetic or decreased vagal tone. This could contribute to increase local coronary hyperreactivity caused by atherosclerotic plaque disruption, thus facilitating progression from unstable angina to acute myocardial infarction (AMI). To test this hypothesis we studied 92 patients admitted to the coronary care unit for episodes of chest pain at rest associated with transient ST shifts (> 0.15 mV). Patients who developed AMI in the first 24 hours, as well as those with previous AMI, concomitant valvular or myocardial diseases or diabetes mellitus were not enrolled in the study. Thirty age-matched subjects without any evidence of coronary artery disease were chosen as controls. All patients underwent a 2 to 5 day continuous Holter monitoring during full medical treatment (including beta-blockers, heparin and aspirin). Angiography was performed within 1 week in 88 of the 92 patients. During follow-up (mean duration of 16 +/- 5 days), 26 patients (Group I) had a major coronary event (6 deaths, 7 non fatal AMI, 13 urgent revascularizations). The remaining 66 patients (Group II) had a good clinical outcome. ECG recordings during ST shifts were excluded from Holter monitoring analysis. Time domain measurements of HRV predicted mortality and total events. The most powerful predictors was the standard deviation of the means of the 5 min R-R intervals (SDANN index) which was significantly (p < 0.001) lower in Group I than Group II (55 +/- 18 versus 87 +/- 29).(ABSTRACT TRUNCATED AT 250 WORDS)

Vasotonic angina: a spectrum of ischemic syndromes involving functional abnormalities of the epicardial and microvascular coronary circulation.

OBJECTIVES: The present study was undertaken to investigate the response of large and small coronary arteries in a subgroup of patients with no or minimal coronary artery disease found to have objective signs of myocardial ischemia. BACKGROUND: Many patients apparently have normal coronary arteries despite abnormal electrocardiographic (ECG) changes during spontaneous anginal attacks or exercise stress testing. METHODS: Twenty-five patients with no or minimal (< 30% stenosis) coronary artery disease were chosen from a pool initially selected on the basis of spontaneous anginal attacks and ST segment shifts in the anterior leads. Of these, 10 were grouped as having variant angina (at least one episode of ST elevation) and the remaining 15 as having syndrome X (exercise-induced anginal pain, ST depression and reversible thallium abnormalities). Data were compared with those obtained in 10 patients with stable angina and documented coronary artery disease. Eighteen patients with supraventricular arrhythmias and normal coronary arteries served as control patients. Patients showing focal spasm during ergonovine testing were not included in the subsequent angiographic analysis. Great cardiac vein blood flow, aortic pressure and changes in coronary artery diameter were measured at rest and 2 to 4 min after hyperventilation in the remaining study group. The same procedure was repeated after sublingual administration of 0.3 mg of nitroglycerin in eight patients (four with syndrome X and four with variant angina). RESULTS: Hyperventilation induced diffuse epicardial coronary diameter reduction, which was marginal in control patients (9 +/- 4%) and those with coronary artery disease (5 +/- 3%) but severe (p < 0.001) in those with variant angina (28 +/- 14%) or syndrome X (25 +/- 13%). Concomitant determination of coronary blood flow showed significant (p < 0.001) decreases in those with variant angina (25 +/- 11%) and syndrome X (28 +/- 10%) but not in control patients (5 +/- 8%) or those with coronary artery disease (4 +/- 5%). Changes in great cardiac vein blood flow during hyperventilation were similar before and after nitroglycerin. CONCLUSIONS: These findings indicate that vasoconstrictor stimuli may trigger a diffuse abnormal response of both epicardial and resistance vessels in some patients with chest pain and angiographically normal coronary arteries. Patients showing such diffuse vasoconstrictor abnormalities are suggested to have a single pathogenetic entity with a spectrum of ECG manifestations ranging from ST depression to ST elevation.